bluuebunny/crossref_metadata_2025_split huggingface dataset:
Behaviour: Role of Genes
Authors: Järvilehto Timo , Lickliter Robert 
Published: September 2009

Abstract

Much effort in behavioural genetics has been motivated by the hope that one day human behaviour will be explicable in genetic terms. This hope is based on the assumption that the contribution of genetic and environmental factors to behaviour can somehow be partitioned. However, recent advances in genomics, cellular and developmental biology, and developmental psychology have made it clear that such partitioning is biologically implausible. The functional significance of genes or any other influence on phenotypic development can be understood only in relation to the organism–environment system of which they are a part. Genes and environments are neither alternative nor independent causes for phenotypic traits.

Key Concepts:

Gene activity is involved in the production of all phenotypic traits.

Partitioning behaviours into those specified by the genes and those that are the result of the environment is not possible.

The causes of behaviour are always relational and distributed across internal and external factors and events.

The influence of any single factor on behaviour (genes, hormones, diet, social interaction) is contingent on the organization of the entire organism–environment system.

Genes do not have a privileged position in the development of behaviour, because they are themselves regulated participants in the developmental process.

Modern developmental theory rejects attempts to separate the organism and environment.
Macrophytes: Ecology of Aquatic Plants
Authors: Bornette Gudrun , Puijalon Sara 
Published: September 2009

Abstract

Aquatic plants contribute to maintaining key functions and related biodiversity in freshwater ecosystems, and to provide the needs of human societies. The way the ecological niches of macrophytes are determined by abiotic filters and biotic ones is considered. A simple, broadly applicable model of the distribution of growth forms according to abiotic filters is proposed. The consequence for the dynamics of plant communities and the main threats to macrophyte occurrence and diversity are discussed.

Key concepts:

Macrophytes contribute to maintaining key functions and related biodiversity in freshwater ecosystems, and to provide the needs of human societies.

Most aquatic species are phylogenetically descended from terrestrial plants that have later adapted to aquatic life.

Water plants are usually poorly lignified, as water preserves plants from gravitational stress, and are characterized by the presence of aerenchyma, which increases oxygen flux from shoots to roots, and by a large leaf surface, together with a thin cuticle, which increase contact with water and carbon uptake.

Macrophyte dispersal relies partly on water drift, and thus on seed buoyancy and on the ability of plants to break themselves up and regrow from broken dispersed fragments, and partly on endozoochory by animals (mainly birds).

In freshwater ecosystems, the production, community composition and life‐history traits of macrophytes are governed by the availability of carbon, nitrogen and phosphorous.

Water movements (waves, flow velocity) tend to select streamlined or prostrate growth forms, and contribute to the dispersal of seeds and vegetative propagules.

Moderate disturbances (by floods or drawdowns) decrease biotic interactions in aquatic plant communities and as a consequence favour biodiversity and decrease successional rate.

Free‐floating and tall species with floating leaves are the most competitive for light, and usually dominate macrophyte communities when nutrient levels in the water are sufficiently high.

In the framework of global change, eutrophication of freshwaters, together with decreases in natural disturbance regimes in river floodplains, increases in groundwater abstraction and the increase of temperature may all contribute in decreasing macrophyte biodiversity by favouring competitive and invasive species, to the detriment of ruderal, stress‐tolerant poorly competitive ones.
Chemolithotrophy
Authors: Oren Aharon 
Published: September 2009

Abstract

Many prokaryotes,
Bacteria
as well as
Archaea
, obtain their energy from the oxidation of reduced inorganic compounds such as hydrogen, ammonia, nitrite, sulfide, elemental sulfur, hydrogen and Fe(II) ions. These organisms can derive all their cellular carbon from carbon dioxide, and they are thus able to grow without any organic compounds and without light. Such microorganisms are called chemolithotrophs or chemoautotrophs. Chemolithotrophic life is possible in the presence as well as in the absence of molecular oxygen. Processes mediated by chemolithotrophic prokaryotes include nitrification (the formation of nitrate from ammonia), production of sulfuric acid from sulfide and elemental sulfur, and the formation of methane from hydrogen and carbon dioxide. Some ecosystems, for example those that develop around deep‐sea hot vents, are entirely driven by carbon fixed by chemolithotrophic microorganisms.

Key concepts

Certain groups of prokaryotes obtain their energy from the oxidation of reduced inorganic compounds such as sulfide, ammonia and hydrogen, and use carbon dioxide as carbon source. These organisms are called chemolithotrophs or chemoautotrophs.

Chemolithotrophy is widespread in the two domains of prokaryotes: the
Bacteria
and the
Archaea
.

Many chemolithotrophs use molecular oxygen as electron acceptor, but chemolithotrophy is also possible in the absence of oxygen. Nitrate, sulfate, elemental sulfur or carbon dioxide serves as electron acceptors for certain groups of chemolithotrophs.

Nitrification, or the oxidation of ammonia via nitrite to nitrate by chemolithotrophic bacteria, is a key process in the global nitrogen cycle.

Two types of anaerobic chemolithotrophs oxidize hydrogen with carbon dioxide as electron acceptor: methanogens and homoacetogens, producing methane and acetate, respectively.

Chemolithotrophs participate in the biogeochemical cycles of certain metals (iron, manganese) and metalloids (arsenic).

In some environments such as deep‐sea hydrothermal vents and certain underground caves, chemolithotrophic primary production driven by the oxidation of hydrogen sulfide provides the basis for the functioning of the ecosystem.
Seed Dispersal
Authors: Nathan Ran , Bullock James M , Ronce Ophélie , Schurr Frank M 
Published: September 2009

AbstractThe sedentary life of adult plants accentuates the critical importance of the short phase during which individual plants move: the dispersal of seeds, a common, widespread and fascinating phenomenon. Ultimately, selective pressures favouring dispersal include inbreeding avoidance, reduction of competition with kin and nonkin and the tracking of establishment opportunities in time and space. Proximately, dispersal mechanisms include nonrandom release from the mother plant, and transport by multiple dispersal vectors not necessarily those inferred from the seed morphology. The resulting patterns, often described by dispersal kernels, typically show a decline in seed deposition with distance from the source and a tail of long‐distance dispersal events. Yet, environmental heterogeneity may cause more complex dispersal patterns. Dispersal has important consequences for the fate of individuals, populations, communities and ecosystems, enabling metapopulations and metacommunities to persist and playing a critical role in shaping the evolutionary and plastic response of plants to changing environments.Key conceptsDispersal is a widespread phenomenon among plants, selected to avoid inbreeding, to reduce competition with kin and nonkin and to cope with spatiotemporally variable environments.Causes for dispersal evolution act in concert, interact and may affect differently the evolution of short‐ and long‐distance dispersal.Seeds typically depart from the source plant in a nonrandom fashion, suggesting selection to coordinate seed release with favourable conditions for dispersal and/or establishment.Seeds of a given plant species are typically dispersed by multiple vectors, including ‘nonstandard’ vectors differing from those inferred from the seed morphology.Dispersal kernels describe how seed deposition varies – in one, two or three spatial dimensions – in relation to the distance from the seed source.One‐dimensional dispersal kernels generally show a decline in seed number (or density) with distance, and a ‘fat’ tail implying more long‐distance dispersal events than expected from a negative exponential distribution.Complex dispersal kernels arise because seed deposition often varies not only with distance but also with direction and environmental heterogeneity.Dispersal plays a key role in allowing plants to adapt to climate changes, to spread within and outside their native range and to maintain metapopulations and metacommunities.New methods to model the underlying mechanisms, to analyze gene flow and genetic structure and to quantify dispersal patterns increase our understanding and predictability of seed dispersal in general, and long‐distance dispersal in particular.
Plant Actin Biology
Authors: Deeks Michael J , Hussey Patrick J 
Published: September 2009

Abstract

Actin is a major component of the plant cytoskeleton. Filamentous actin (F‐actin) contributes to the maintenance of the internal architecture of the cell, drives cytoplasmic streaming (the movement of components around the cytosol) and contributes to the process of cell division. The biochemistry of plant actin has many similarities to that of yeast and animals, but has developed its own strategies and molecular machinery to organize actin filaments. F‐actin provides tracks for myosin molecular motors to transport organelles at high velocities and actin is required for specific stages of vesicle trafficking that underpin cell growth and development. The means by which plant cells control the nucleation of new actin filaments from G‐actin have diverged considerably from yeast and metazoans. The unique aspects of the plant actin cytoskeleton are likely to have arisen from a combination of the environmental challenges to a sessile multicellular existence and a complex evolutionary history.

Key concepts

The basic principles of actin biochemistry applicable to animals, fungi and protists are conserved in plants but there are a number of specific modifications as plants do not possess the full complement of animal actin‐binding proteins.

Actin filaments in plants have to fulfil unique functions. Actin focuses on the expansion of tip growing cells, maintains cytoarchitecture and responds to the environment (e.g. polarizing in response to pathogen stimulation). During cell division actin filaments participate in all major plant‐specific arrays.

A stationary cell is NOT a physically inactive cell. Actin cables are exploited for organelle transport. Actin‐based transport tends to dominate over microtubule‐based movement. Plants utilize the fastest known type V myosin (known in plants as type XI) within the eukaryote kingdom. Polymerization dynamics are thought to add to trafficking capabilities as low levels of antiactin drugs disrupt vesicle delivery and fusion during cell growth yet preserve myosin‐mediated transport.

New proteins and new domain combinations have become established in plants to regulate the actin cytoskeleton in accordance with the unusual demands placed on them. Importantly, these radical adaptations should not be considered purely in terms of a response to a sedentary way of life as the fungal kingdom has achieved such a conversion using arguably less radical cytoskeletal solutions. Consequently the impact of other unique facets of plant evolutionary history and niches must be considered.
The Rust Fungi
Authors: Kolmer James A , Ordonez Maria E , Groth James V 
Published: September 2009

AbstractThe rust fungi are a monophyletic group of approximately 7000 species in the basidiomycota and are highly specialized obligate parasites of plants. The life cycle of rusts can be complex. Some rusts have up to five spore stages that alternate between haploid and dikaryotic nuclear conditions and that can occur on two taxonomically unrelated host plants. The rusts have evolved specialized structures that allow them to penetrate and obtain nutrients from living host cells. Biologic forms of a single rust species may differ in ability to attack different genera of host plants. Furthermore, within a single rust species they can be highly variable in ability to attack different genotypes of one host species. At the species level, genes that condition avirulence/virulence in rusts interact in a specific relationship with rust‐resistance genes in plants. Many of the most important plant diseases in the world are caused by rust fungi.Key concepts:The rust fungi are a monophyletic group of approximately 7000 species within the basidiomycota, the group of fungi that includes mushrooms and shelf fungi.Rust fungi have complex life cycles with up to five spore stages that alternate between haploid and dikaryotic nuclear condition on two unrelated host plants.The rust fungi are obligate parasites of plants and have evolved specialized structures to infect and obtain nutrients from plants.Rusts have a highly specific host range. Genes in rust that express avirulence or virulence interact with rust‐resistance genes in host plants to condition a compatible or incompatible interaction. Some rust species are highly variable for biologic forms that vary in their ability to attack host genotypes with different rust‐resistance genes.Many of the most important plant diseases worldwide are caused by rust fungi.
Sleep and Memory
Authors: Aton SJ , Seibt J , Frank MG 
Published: September 2009

Abstract

Current behavioural evidence indicates that sleep plays a central role in memory consolidation. Neural events during post‐learning sleep share key features with both early and late stages of memory consolidation. For example, recent studies have shown neuronal changes during post‐learning sleep which reflect early synaptic changes associated with consolidation, including activation of shared intracellular pathways and modifications of synaptic strength. Sleep may also play a role in later stages of consolidation involving propagation of memory traces throughout the brain. However, to date the precise molecular and physiological aspects of sleep required for this process remain unknown. The behavioural effects of sleep may be mediated by the large‐scale, global changes in neuronal activity, synchrony and intracellular communication that accompany this vigilance state, or by synapse‐specific ‘replay’ of activity patterns associated with prior learning.

Key concepts

Memory consolidation involves plastic changes at the synaptic and brain systems levels; these changes occur over timescales of minutes (synaptic consolidation) to days or months (systems consolidation).

Cellular changes occurring during early post‐learning sleep suggest that synaptic consolidation may occur preferentially during sleep.

Brain‐imaging and gene‐expression studies have provided limited evidence that sleep may facilitate the gradual redistribution of memory traces throughout the brain.

Sleep may facilitate consolidation through large‐scale changes in neural activity, neurotransmission or gene expression associated with rapid eye movement (REM) and non‐REM (NREM) vigilance states.

It remains unclear whether sleep‐dependent consolidation is mediated by permissive (global) or instructive (synapse‐specific) mechanisms.
Memory: Mechanisms Other than
LTP
Authors: Debanne Dominique , Campanac Emilie 
Published: September 2009

Abstract

Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage. Long‐term changes in neuronal excitability have been reported in several brain areas following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Similarly to synaptic plasticity, long‐lasting intrinsic plasticity is bidirectional and expresses a certain level of input or cell specificity. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.

Key concepts:
Synaptic plasticity is not the exclusive mode of memory storage, and persistent regulation of voltage‐gated ionic channels also participates in information storage following learning. Synaptic activation of glutamate receptors initiates long‐lasting modification in neuronal excitability at the pre‐ or postsynaptic side. Intrinsic plasticity is mediated by changes in the expression level or biophysical properties of ion channels in the membrane and can affect many different neuronal operations such as dendritic integration and action potential generation and propagation. Synaptic and intrinsic plasticities not only share common learning rules and induction pathways but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram.
Learning Disorders: Beyond Dyslexia
Authors: Banai Karen , Yifat Rachel 
Published: September 2009

Abstract

Learning disabilities (LD) – the unexpected academic difficulties experienced by many otherwise typically developing persons – are highly heterogeneous in nature. Thus, while at the academic level 80–90% of individuals with LD suffer from poor reading fluency and/or accuracy, at the cognitive level multiple processes are implicated including language, attention, perception and memory. Similarly, at the biological level many brain systems and processes are affected. In the auditory system alone, individuals with LD were shown to process sound abnormally at all levels of the auditory pathway from the brainstem to high level cortical areas. Taken together, current research suggests that a single core deficit model is unlikely to account for the aetiology of LD and furthermore, that the observed pattern of academic strengths and weaknesses is affected little by differences in underlying processes. Therefore, it appears that different underlying vulnerabilities result in similar academic outcomes.

Key Concepts

Physiological and perceptual processing of the acoustic elements of sound such as its duration, frequency, rate of presentation, etc.

The concurrent occurrence of two disorders. In the present context, an individual diagnosed with LD is more likely to be diagnosed with another form of learning or attention disorder compared to an undiagnosed individual.

Disorders that involve the processing of linguistic information such as phonology, grammar and semantics. May reflect difficulties in expression, comprehension or both.

A mental representation of recently perceived stimuli that can be used to ease the perception of ongoing stimuli.

Processes related to the linguistic analysis of the basic units of speech such as the ability to segment words to syllables, phonemes or units that are thought to structure sound to convey linguistic meaning, or to remember a string of speech sounds in short‐term memory.

The ability to perform cognitive operations (e.g. repeating in backwards order) on items held in short‐term memory.
Gaucher Disease
Authors: Germain Dominique P 
Published: September 2009

Abstract

Gaucher disease (GD) is a lysosomal storage disorder due to deficiency in acid β‐glucosidase. Partial enzyme deficiency is associated with parenchymal disease of the liver, spleen and bone marrow in non‐neuronopathic, type 1 GD, while complete deficiency, caused by severe mutations in the

GBA

gene, is additionally associated with neurological manifestations in type 2 and type 3 GD. Specific therapy is available for GD: enzyme replacement therapy has proven safe and effective and is the current standard of care for type 1 GD but cannot reverse the neurological deficits in type 2 or type 3. New recombinant enzymes are currently in clinical trials. Small‐molecule inhibitors of
glucosylceramide synthase
are both available and being developed for substrate reduction therapy. Active‐site‐specific pharmacological chaperones and gene therapy are being explored as other potential therapeutic options.

Key concepts:

Gaucher disease (GD) is an autosomal recessive inborn error of sphingolipid metabolism due to the deficient activity of the lysosomal enzyme acid β‐glucosidase.

Three phenotypes of GD are conventionally distinguished on the basis of the absence (type 1) or presence and severity (types 2 and 3) of central nervous system involvement.

Patients with type 1 GD may present with splenomegaly, hepatomegaly, radiologic bone disease, thrombocytopaenia, anaemia and bone pain.

A higher incidence of multiple myeloma in GD has been reported and patients should have their immunoglobulin profile determined at diagnosis and monitored every 2 years.

The natural course of GD varies widely, with some subjects remaining asymptomatic up to the age of 70 or 80 years, in contrast to the sometimes fatal progression in childhood. This emphasizes the need for a regular follow‐up to enable timely initiation of enzyme therapy.

The demonstration of a deficient activity of acid β‐glucosidase activity in leukocytes is the reference laboratory method which should be used to confirm the clinical diagnosis of GD.

Enzyme replacement therapy (ERT) with imiglucerase is central to modern management of GD. The aim of ERT is to achieve reversal of the symptomatic clinical manifestations and prevent irreversible lesions of the various organs.

Over 3500 patients are receiving treatment worldwide, with a maximum follow‐up of 15 years. The therapeutic results have been the subject of several analyses. The response to ERT is generally excellent, although marked inter‐individual variability exists. ERT is safe and well tolerated.

Substrate reduction therapy (miglustat) reduces tissue glycosphingolipid storage by limiting the amount of the precursor synthesized to a level that can be cleared by the mutant enzyme with residual hydrolytic activity.

Since the neurological forms of GD do not respond to ERT, further research on other therapeutic strategies including gene therapy, substrate reduction therapy and chaperone therapy is warranted.
The
BCL
‐2 Family Proteins – Key Regulators and Effectors of Apoptosis
Authors: Vaux David L 
Published: September 2009

Abstract

BCL‐2 was the first cloned component of the mechanism for apoptosis – the process by which metazoan cells commit suicide – to be recognized. Mammals are now known to carry genes for a large number of BCL‐2 like proteins, some of which, like BCL‐2 itself, inhibit apoptosis, and others that promote or are required for apoptosis. Direct interactions between BCL‐2 family members are essential for the proper regulation and implementation of apoptosis during development and for homoeostasis. Abnormalities to the regulation of cell death, such as those caused by mutations to genes for BCL‐2 family members prevent apoptosis occurring when it should, and can lead to diseases including cancer. Understanding the roles of BCL‐2 family members, their structures and how they interact, has allowed the development of novel agents for the treatment of cancer that are now in clinical trials.

Key concepts

A major mechanism by which mammalian cells kill themselves involves members of the BCL‐2 family of proteins, some of which promote cell death, and others which inhibit cell death.

BCL‐2 family proteins interact with each other to regulate and implement the cell death programme.

Abnormalities to the regulation of this cell death process, including mutations to genes for BCL‐2 family members, can lead to a disease, such as cancer.