Question: What animals rhythmic feeding times were studied in the early 20th century ?

Answer: bees

In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. <hl> In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees . <hl> Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.

In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of <hl> bees <hl>. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.

In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of <hl> bees <hl> .

question: What animals rhythmic feeding times were studied in the early 20th century ?, context: In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.


Question: What gene did Konopka and Benzer map in the early 1970 s?

Answer: "period"

In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. <hl> Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. <hl> Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.

In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the <hl> "period" <hl> gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.

question: What gene did Konopka and Benzer map in the early 1970 s?, context: In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.


Question: What mutation did Takahashi discover in 1994?

Answer: circadian clock

In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. <hl> Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. <hl> However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.

In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian <hl> circadian clock <hl> mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.

question: What mutation did Takahashi discover in 1994?, context: In 1896, Patrick and Gilbert observed that during a prolonged period of sleep deprivation, sleepiness increases and decreases with a period of approximately 24 hours. In 1918, J.S. Szymanski showed that animals are capable of maintaining 24-hour activity patterns in the absence of external cues such as light and changes in temperature. In the early 20th century, circadian rhythms were noticed in the rhythmic feeding times of bees. Extensive experiments were done by Auguste Forel, Ingeborg Beling, and Oskar Wahl to see whether this rhythm was due to an endogenous clock.[citation needed] Ron Konopka and Seymour Benzer isolated the first clock mutant in Drosophila in the early 1970s and mapped the "period" gene, the first discovered genetic determinant of behavioral rhythmicity. Joseph Takahashi discovered the first mammalian circadian clock mutation (clockΔ19) using mice in 1994. However, recent studies show that deletion of clock does not lead to a behavioral phenotype (the animals still have normal circadian rhythms), which questions its importance in rhythm generation.


Question: Inside of what can the molecular circadian clock operate?

Answer: single cell

<hl> It is now known that the molecular circadian clock can function within a single cell ; i.e., it is cell-autonomous. <hl> This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

It is now known that the molecular circadian clock can function within a <hl> single cell <hl>; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

It is now known that the molecular circadian clock can function within a <hl> single cell <hl> ; i.e., it is cell-autonomous.

question: Inside of what can the molecular circadian clock operate?, context: It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]


Question: By functioning within a single, what is the system?

Answer: cell-autonomous

<hl> It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous . <hl> This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

It is now known that the molecular circadian clock can function within a single cell; i.e., it is <hl> cell-autonomous <hl>. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

It is now known that the molecular circadian clock can function within a single cell; i.e., it is <hl> cell-autonomous <hl> .

question: By functioning within a single, what is the system?, context: It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]


Question: What section of the brain periodically releases hormones?

Answer: endocrine glands

It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. <hl> These may interface with endocrine glands of the brain to result in periodic release of hormones. <hl> The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with <hl> endocrine glands <hl> of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

question: What section of the brain periodically releases hormones?, context: It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]


Question: How are sleep and wake cycles as well as body functions coordinated?

Answer: biological clock

It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. <hl> This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock .[citation needed] <hl>

It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the <hl> biological clock <hl>.[citation needed]

This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the <hl> biological clock <hl> .[citation needed]

question: How are sleep and wake cycles as well as body functions coordinated?, context: It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]


Question: What do body hormone receptors do with the body's organs?

Answer: synchronise

It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in <hl> a synchronise d output of electrical signaling. <hl> These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a <hl> synchronise <hl>d output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]

a <hl> synchronise <hl> d output of electrical signaling.

question: What do body hormone receptors do with the body's organs?, context: It is now known that the molecular circadian clock can function within a single cell; i.e., it is cell-autonomous. This was shown by Gene Block in isolated mollusk BRNs.[clarification needed] At the same time, different cells may communicate with each other resulting in a synchronised output of electrical signaling. These may interface with endocrine glands of the brain to result in periodic release of hormones. The receptors for these hormones may be located far across the body and synchronise the peripheral clocks of various organs. Thus, the information of the time of the day as relayed by the eyes travels to the clock in the brain, and, through that, clocks in the rest of the body may be synchronised. This is how the timing of, for example, sleep/wake, body temperature, thirst, and appetite are coordinately controlled by the biological clock.[citation needed]


Question: What signals plants to synchronize their internal clocks?

Answer: Light

<hl> Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. <hl> Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

<hl> Light <hl> is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

question: What signals plants to synchronize their internal clocks?, context: Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.


Question: What do plants use to sense light?

Answer: photoreceptors

<hl> Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors . <hl> Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of <hl> photoreceptors <hl>. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of <hl> photoreceptors <hl> .

question: What do plants use to sense light?, context: Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.


Question: What receptors absorb red and blue light in plants?

Answer: phytochromes and cryptochromes

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. <hl> Red and blue light are absorbed through several phytochromes and cryptochromes . <hl> One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several <hl> phytochromes and cryptochromes <hl>. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Red and blue light are absorbed through several <hl> phytochromes and cryptochromes <hl> .

question: What receptors absorb red and blue light in plants?, context: Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.


Question: Which phytochrome found in seedlings deteriorates with light and growth?

Answer: phyA

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. <hl> One phytochrome, phyA , is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. <hl> Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, <hl> phyA <hl>, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

One phytochrome, <hl> phyA <hl> , is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1.

question: Which phytochrome found in seedlings deteriorates with light and growth?, context: Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.


Question: What is the main phytochrome found in seedling grown in light?

Answer: phyB

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. <hl> Phytochromes B–E are more stable with phyB , the main phytochrome in seedlings grown in the light. <hl> The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with <hl> phyB <hl>, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.

Phytochromes B–E are more stable with <hl> phyB <hl> , the main phytochrome in seedlings grown in the light.

question: What is the main phytochrome found in seedling grown in light?, context: Light is the signal by which plants synchronize their internal clocks to their environment and is sensed by a wide variety of photoreceptors. Red and blue light are absorbed through several phytochromes and cryptochromes. One phytochrome, phyA, is the main phytochrome in seedlings grown in the dark but rapidly degrades in light to produce Cry1. Phytochromes B–E are more stable with phyB, the main phytochrome in seedlings grown in the light. The cryptochrome (cry) gene is also a light-sensitive component of the circadian clock and is thought to be involved both as a photoreceptor and as part of the clock's endogenous pacemaker mechanism. Cryptochromes 1–2 (involved in blue–UVA) help to maintain the period length in the clock through a whole range of light conditions.


Question: What time cycle did studies in 1938 and 1990s use on humans?

Answer: 28-hour

<hl> Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. <hl> Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced <hl> 28-hour <hl> sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

question: What time cycle did studies in 1938 and 1990s use on humans?, context: Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]


Question: What conditions were suppressed in the 28 hour wake-sleep cycle studies ?

Answer: time cues

<hl> Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. <hl> Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other <hl> time cues <hl> suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

question: What conditions were suppressed in the 28 hour wake-sleep cycle studies ?, context: Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]


Question: How long did the suppression of time clues study last?

Answer: month

<hl> Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month . <hl> Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a <hl> month <hl>. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a <hl> month <hl> .

question: How long did the suppression of time clues study last?, context: Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]


Question: What is this forced type of study called?

Answer: forced desynchrony

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. <hl> Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. <hl> Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a <hl> forced desynchrony <hl> protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

question: What is this forced type of study called?, context: Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]


Question: When in the cycle do wake-sleep cycles break off from the circadian period?

Answer: 24.18 hours

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. <hl> Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed] <hl>

Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about <hl> 24.18 hours <hl> and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]

question: When in the cycle do wake-sleep cycles break off from the circadian period?, context: Studies by Nathaniel Kleitman in 1938 and by Derk-Jan Dijk and Charles Czeisler in the 1990s put human subjects on enforced 28-hour sleep–wake cycles, in constant dim light and with other time cues suppressed, for over a month. Because normal people cannot entrain to a 28-hour day in dim light if at all,[citation needed] this is referred to as a forced desynchrony protocol. Sleep and wake episodes are uncoupled from the endogenous circadian period of about 24.18 hours and researchers are allowed to assess the effects of circadian phase on aspects of sleep and wakefulness including sleep latency and other functions.[page needed]


Question: What effect does jet-lag and shift-work have on the human body?

Answer: profound consequences

<hl> Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. <hl> Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

Shift-work or chronic jet-lag have <hl> profound consequences <hl> on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

question: What effect does jet-lag and shift-work have on the human body?, context: Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.


Question: Animals that eat during resting periods show what body increase?

Answer: body mass

Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. <hl> Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] <hl> In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased <hl> body mass <hl> and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

question: Animals that eat during resting periods show what body increase?, context: Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.


Question: How does irregular eating during shift-work effect insulin?

Answer: insulin sensitivity

Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] <hl> In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. <hl> Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered <hl> insulin sensitivity <hl> and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

question: How does irregular eating during shift-work effect insulin?, context: Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.


Question: Besides insulin sensitivity, what other effect does shift-work have on the body?

Answer: higher body mass

Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] <hl> In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass . <hl> Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and <hl> higher body mass <hl>. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and <hl> higher body mass <hl> .

question: Besides insulin sensitivity, what other effect does shift-work have on the body?, context: Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.


Question: What type of work can lead to heart, hypertension and inflammation?

Answer: Shift-work

<hl> Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. <hl> Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

<hl> Shift-work <hl> or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.

question: What type of work can lead to heart, hypertension and inflammation?, context: Shift-work or chronic jet-lag have profound consequences on circadian and metabolic events in the body. Animals that are forced to eat during their resting period show increased body mass and altered expression of clock and metabolic genes.[medical citation needed] In humans, shift-work that favors irregular eating times is associated with altered insulin sensitivity and higher body mass. Shift-work also leads to increased metabolic risks for cardio-metabolic syndrome, hypertension, inflammation.


Question: What do studies show has a bidirectional relationship with the circadian system?

Answer: abusive drugs

<hl> Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs . <hl> It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and <hl> abusive drugs <hl>. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and <hl> abusive drugs <hl> .

question: What do studies show has a bidirectional relationship with the circadian system?, context: Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.


Question: What do abusive drugs effect in the circadian system?

Answer: circadian pacemaker

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. <hl> It is indicated that these abusive drugs affect the central circadian pacemaker . <hl> Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central <hl> circadian pacemaker <hl>. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

It is indicated that these abusive drugs affect the central <hl> circadian pacemaker <hl> .

question: What do abusive drugs effect in the circadian system?, context: Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.


Question: What do drug abusers show in their circadian processes?

Answer: disrupted rhythms

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. <hl> Individuals suffering from substance abuse display disrupted rhythms . <hl> These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display <hl> disrupted rhythms <hl>. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

Individuals suffering from substance abuse display <hl> disrupted rhythms <hl> .

question: What do drug abusers show in their circadian processes?, context: Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.


Question: What can the disrupted circadian system cause?

Answer: abuse and relapse

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. <hl> These disrupted rhythms can increase the risk for substance abuse and relapse . <hl> It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance <hl> abuse and relapse <hl>. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.

These disrupted rhythms can increase the risk for substance <hl> abuse and relapse <hl> .

question: What can the disrupted circadian system cause?, context: Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.


Question: What can disruption to genetics and environment in the sleep cycle cause?

Answer: susceptibility to addiction

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. <hl> It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction . <hl>

Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the <hl> susceptibility to addiction <hl>.

It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the <hl> susceptibility to addiction <hl> .

question: What can disruption to genetics and environment in the sleep cycle cause?, context: Studies conducted on both animals and humans show major bidirectional relationships between the circadian system and abusive drugs. It is indicated that these abusive drugs affect the central circadian pacemaker. Individuals suffering from substance abuse display disrupted rhythms. These disrupted rhythms can increase the risk for substance abuse and relapse. It is possible that genetic and/or environmental disturbances to the normal sleep and wake cycle can increase the susceptibility to addiction.


Question: What is theorized to have evolved with circadian rhythms?

Answer: photosensitive proteins

What drove circadian rhythms to evolve has been an enigmatic question. <hl> Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. <hl> As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that <hl> photosensitive proteins <hl> and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

question: What is theorized to have evolved with circadian rhythms?, context: What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.


Question: What is thought that circadian rhythm evolved to protect?

Answer: replicating DNA

What drove circadian rhythms to evolve has been an enigmatic question. <hl> Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. <hl> As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting <hl> replicating DNA <hl> from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

question: What is thought that circadian rhythm evolved to protect?, context: What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.


Question: From what did DNA need to be protected in the earliest cells?

Answer: ultraviolet radiation

What drove circadian rhythms to evolve has been an enigmatic question. <hl> Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. <hl> As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging <hl> ultraviolet radiation <hl> during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

question: From what did DNA need to be protected in the earliest cells?, context: What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.


Question: One possible reason for the development of the circadian system is the need to counteract what ?

Answer: redox reactions

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. <hl> The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis. <hl>

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging <hl> redox reactions <hl> on a daily basis.

question: One possible reason for the development of the circadian system is the need to counteract what ?, context: What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.


Question: What environmental event occurred 2.3 million years ago?

Answer: Great Oxidation Event

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. <hl> Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. <hl> The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the <hl> Great Oxidation Event <hl> approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.

question: What environmental event occurred 2.3 million years ago?, context: What drove circadian rhythms to evolve has been an enigmatic question. Previous hypotheses emphasized that photosensitive proteins and circadian rhythms may have originated together in the earliest cells, with the purpose of protecting replicating DNA from high levels of damaging ultraviolet radiation during the daytime. As a result, replication was relegated to the dark. However, evidence for this is lacking, since the simplest organisms with a circadian rhythm, the cyanobacteria, do the opposite of this - they divide more in the daytime. Recent studies instead highlight the importance of co-evolution of redox proteins with circadian oscillators in all three kingdoms of life following the Great Oxidation Event approximately 2.3 billion years ago. The current view is that circadian changes in environmental oxygen levels and the production of reactive oxygen species (ROS) in the presence of daylight are likely to have driven a need to evolve circadian rhythms to preempt, and therefore counteract, damaging redox reactions on a daily basis.


Question: What is the body clock gene in animals necessary to ensure?

Answer: cellular/metabolic events

<hl> Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events ; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. <hl> In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of <hl> cellular/metabolic events <hl>; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of <hl> cellular/metabolic events <hl> ; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism.

question: What is the body clock gene in animals necessary to ensure?, context: Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.


Question: What do mice without the clock gene become?

Answer: hyperphagic and obese

<hl> Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese , and have altered glucose metabolism. <hl> In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are <hl> hyperphagic and obese <hl>, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are <hl> hyperphagic and obese <hl> , and have altered glucose metabolism.

question: What do mice without the clock gene become?, context: Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.


Question: Beside obesity, how else does the lack of a circadian clock effect the mice?

Answer: glucose metabolism

<hl> Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism . <hl> In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered <hl> glucose metabolism <hl>. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered <hl> glucose metabolism <hl> .

question: Beside obesity, how else does the lack of a circadian clock effect the mice?, context: Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.


Question: How certain is it that these circadian clock effects are the same in humans?

Answer: not clear

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. <hl> However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome. <hl>

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is <hl> not clear <hl> whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

question: How certain is it that these circadian clock effects are the same in humans?, context: Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.


Question: What gene needs to be deleted to cause obesity in mice?

Answer: Rev-ErbA alpha clock

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. <hl> In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. <hl> However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the <hl> Rev-ErbA alpha clock <hl> gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.

question: What gene needs to be deleted to cause obesity in mice?, context: Mutations or deletions of clock gene in mice have demonstrated the importance of body clocks to ensure the proper timing of cellular/metabolic events; clock-mutant mice are hyperphagic and obese, and have altered glucose metabolism. In mice, deletion of the Rev-ErbA alpha clock gene facilitates diet-induced obesity and changes the balance between glucose and lipid utilization predisposing to diabetes. However, it is not clear whether there is a strong association between clock gene polymorphisms in humans and the susceptibility to develop the metabolic syndrome.


Question: Where is the primary circadian gene located in humans?

Answer: suprachiasmatic nucleus

<hl> The primary circadian "clock" in mammals is located in the suprachiasmatic nucleus (or nuclei) (SCN), a pair of distinct groups of cells located in the hypothalamus. <hl> Destruction of the SCN results in the complete absence of a regular sleep–wake rhythm. The SCN receives information about illumination through the eyes. The retina of the eye contains "classical" photoreceptors ("rods" and "cones"), which are used for conventional vision. But the retina also contains specialized ganglion cells that are directly photosensitive, and project directly to the SCN, where they help in the entrainment (synchronization) of this master circadian clock.

The primary circadian "clock" in mammals is located in the <hl> suprachiasmatic nucleus <hl> (or nuclei) (SCN), a pair of distinct groups of cells located in the hypothalamus. Destruction of the SCN results in the complete absence of a regular sleep–wake rhythm. The SCN receives information about illumination through the eyes. The retina of the eye contains "classical" photoreceptors ("rods" and "cones"), which are used for conventional vision. But the retina also contains specialized ganglion cells that are directly photosensitive, and project directly to the SCN, where they help in the entrainment (synchronization) of this master circadian clock.

question: Where is the primary circadian gene located in humans?, context: The primary circadian "clock" in mammals is located in the suprachiasmatic nucleus (or nuclei) (SCN), a pair of distinct groups of cells located in the hypothalamus. Destruction of the SCN results in the complete absence of a regular sleep–wake rhythm. The SCN receives information about illumination through the eyes. The retina of the eye contains "classical" photoreceptors ("rods" and "cones"), which are used for conventional vision. But the retina also contains specialized ganglion cells that are directly photosensitive, and project directly to the SCN, where they help in the entrainment (synchronization) of this master circadian clock.


Question: Where are these cell groups found in humans?

Answer: hypothalamus

<hl> The primary circadian "clock" in mammals is located in the suprachiasmatic nucleus (or nuclei) (SCN), a pair of distinct groups of cells located in the hypothalamus . <hl> Destruction of the SCN results in the complete absence of a regular sleep–wake rhythm. The SCN receives information about illumination through the eyes. The retina of the eye contains "classical" photoreceptors ("rods" and "cones"), which are used for conventional vision. But the retina also contains specialized ganglion cells that are directly photosensitive, and project directly to the SCN, where they help in the entrainment (synchronization) of this master circadian clock.

The primary circadian "clock" in mammals is located in the suprachiasmatic nucleus (or nuclei) (SCN), a pair of distinct groups of cells located in the <hl> hypothalamus <hl>. Destruction of the SCN results in the complete absence of a regular sleep–wake rhythm. The SCN receives information about illumination through the eyes. The retina of the eye contains "classical" photoreceptors ("rods" and "cones"), which are used for conventional vision. But the retina also contains specialized ganglion cells that are directly photosensitive, and project directly to the SCN, where they help in the entrainment (synchronization) of this master circadian clock.

The primary circadian "clock" in mammals is located in the suprachiasmatic nucleus (or nuclei) (SCN), a pair of distinct groups of cells located in the <hl> hypothalamus <hl> .

question: Where are these cell groups found in humans?, context: The primary circadian "clock" in mammals is located in the suprachiasmatic nucleus (or nuclei) (SCN), a pair of distinct groups of cells located in the hypothalamus. Destruction of the SCN results in the complete absence of a regular sleep–wake rhythm. The SCN receives information about illumination through the eyes. The retina of the eye contains "classical" photoreceptors ("rods" and "cones"), which are used for conventional vision. But the retina also contains specialized ganglion cells that are directly photosensitive, and project directly to the SCN, where they help in the entrainment (synchronization) of this master circadian clock.