nirantk/geneticsQA-train huggingface dataset:
Question: In which kingdom do microsporidia belong, according to their current classification scheme?

Context:
Microsporidia are a diverse group of obligate, intracellular, eukaryotic, spore-forming parasites. Traditionally, these were considered as protozoans but recently have been reclassified as fungi. 
Microsporidia are ubiquitous fungi with genomes that have undergone a strong reduction
Microsporidia are unicellular fungi that are obligate endoparasites. 
Phylogenomics supports microsporidia as the earliest diverging clade of sequenced fungi.
A combined analysis of thousands of gene trees supports a topology in which microsporidia is a sister group to all other sequenced fungi.
Altogether, our data strongly support a scenario in which microsporidia is the earliest-diverging clade of sequenced fungi.
Microsporidia are a large diverse group of intracellular parasites now considered as fungi.
The unique genomic hallmarks between microsporidia and fungi are independent of sequence based phylogenetic comparisons and further contribute to define the borders of the fungal kingdom and support the classification of microsporidia as unusual derived fungi.
The kingdom Fungi is expanded by adding Microsporidia, because of protein sequence evidence that these amitochondrial intracellular parasites are related to conventional Fungi, not Protozoa.
The preponderance of evidence as to the origin of the microsporidia reveals a close relationship with the fungi, either within the kingdom or as a sister group to it.
In a subsequent analysis, we excluded the other Microsporidia from the analysis to look for relationships before the divergence of Microsporidia, and found that 43% of the microsporidial genes scored highest with fungal genes, and a higher mean LPI was found with Fungi than with other kingdoms, suggesting that Microsporidia is closely related to Fungi at the genomic level.
CONCLUSION/SIGNIFICANCE: The unique genomic hallmarks between microsporidia and fungi are independent of sequence based phylogenetic comparisons and further contribute to define the borders of the fungal kingdom and support the classification of microsporidia as unusual derived fungi.
The unique genomic hallmarks between microsporidia and fungi are independent of sequence based phylogenetic comparisons and further contribute to define the borders of the fungal kingdom and support the classification of microsporidia as unusual derived fungi.
The kingdom Fungi is expanded by adding Microsporidia, because of protein sequence evidence that these amitochondrial intracellular parasites are related to conventional Fungi, not Protozoa.
Microorganisms of the microsporidia group are obligated intracellular protozoa that belong to the phylum Microspora; currently they are considered to be related or belong to the fungi reign

Answer: Traditionally, microsporidia were considered as protozoans, but recently they have been reclassified as the earliest-diverging clade of sequenced fungi. Microsporidia are a diverse group of obligate, intracellular, eukaryotic, spore-forming parasites; they are ubiquitous fungi, with genomes that have undergone a strong reduction.
Exact answer: Fungi
Question: What is the effect induced by sympathetic nervous system on pupil size?

Context:
Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system.
The sympathetic nervous system acts either directly on the dilator muscle (peripherally) or centrally by inhibiting the Edinger-Westphal nucleus.
The mechanism of reflex pupillary dilation was investigated in eight patients who were declared brain dead after rupture of intracranial vascular malformations and in eight awake volunteers. The authors hypothesized that the reflex was primarily a spinal sympathetic reflex
The authors conclude that pupillary reflex dilation, as it is clinically performed in awake subjects by stimulating somatic nociceptors, is a sympathetic reflex.
Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system.
Sympathetic nervous system activation, with reflex dilation of the pupil
reproducibly larger pupil size--indicative of increased sympathetic arousal--
activation of autonomic sympathetic preganglionic neurons in the thoracic spinal cord produces pupillary dilatation
sympathetic responses (sweating, pupil dilatation, piloerection, etc.)
In the absence of anesthesia, dilation is primarily mediated by the sympathetic nervous system.
Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system.
Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration.
BACKGROUND: Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system.
Dark-adapted pupil size after topical PNS blockade (an index of iris sympathetic nervous system [SNS] activity) was also smaller in both groups of diabetic subjects (NIDD, P less than 0.01; IDD, P less than 0.05).
However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001).
However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001)
Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system
Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system

Answer: Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system. The sympathetic nervous system acts either directly on the dilator muscle (peripherally) or centrally by inhibiting the Edinger-Westphal nucleus. Thus, the sympathetic nervous system mediates pupillary dilatation.
Exact answer: pupillary dilatation (increase of the pupil size)
Question: Has overexpression of sirtuins been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae)?

Context:
In addition, Sir2 overexpression prevents Rif1 deletion from disrupting Sir2 at IGS1 and shortening lifespan. 
Roles for sirtuin proteins at telomeres are thought to promote lifespan in yeast and mammals.
Overexpression of sirtuins (NAD(+)-dependent protein deacetylases) has been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae)
When overexpressed, the NAD-dependent protein deacetylase Sir2 extends the lifespan of both budding yeast 
When overexpressed in primary mouse embryo fibroblasts (MEFs), SIRT1 antagonizes PML-induced acetylation of p53 and rescues PML-mediated premature cellular senescence. 

Answer: Overexpression of sirtuins (NAD(+)-dependent protein deacetylases) has been reported to increase lifespan in budding yeast (Saccharomyces cerevisiae).
Exact answer: yes
Question: Which histone marks are deposited by Set7?

Context:
the loss of H4 lysine 20 methylation
Transcriptionally competent regions lack H4 lysine 20 methylation
a human histone H4 lysine 20 methyltransferase and cloned the encoding gene, PR/SET07
Localization of PR-Set7 to mitotic chromosomes and subsequent increase in H4 Lys 20 methylation
the H4-K20 methyltransferase PR-Set7. Indeed, upregulation of PR-Set7 expression upon loss of HCF-1 leads to improper mitotic H4-K20 methylation

Answer: Set7 is H4K20 monomethyltransferase. Upregulation of PR-Set7 expression upon loss of HCF-1 leads to improper mitotic H4-K20 methylation. Set7 (or some variant) has also been reported to perform mono-methylation on lysine-4 of H3.
Exact answer: H4K20 monomethylation, H3K4 monomethylation
Question: Which is the process that Conserved noncoding elements mostly regulate?

Context:
Much evidence suggests that CNEs are selectively constrained and not mutational cold-spots, and there is evidence that some CNEs play a role in the regulation of development.
This result suggests that there is widespread adaptation in mammalian conserved noncoding DNA elements, some of which have been implicated in the regulation of crucially important processes, including development.
Some characteristics of CNEs include their high frequency in mammalian genomes, their potential regulatory role in gene expression, and their enrichment in gene deserts nearby master developmental genes
Animal genomes possess highly conserved cis-regulatory sequences that are often found near genes that regulate transcription and development.
HCNEs of both human and zebrafish function as specific developmental enhancers in zebrafish.
HCNEs from the same area often drive overlapping patterns, suggesting that multiple regulatory inputs are required to achieve robust and precise complex expression patterns exhibited by developmental genes.
These results suggest important roles for SINEs in the development of the mammalian neuronal network, a part of which was initiated with the exaptation of AmnSINE1 in a common mammalian ancestor.
Further positional analysis of these conserved noncoding elements (CNEs) in the genome demonstrates that they cluster around genes involved in developmental regulation.
The majority of tetrapod-specific UCEs are noncoding and associated with genes involved in regulation of transcription and development.
Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with genes involved in transcriptional regulation of development
In 74% of cases, we were able to assign a specific set of paralogous genes with annotation relating to transcriptional regulation and/or development to each family
The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important transcription factors (TFs). This suggests that HCNE-rich regions may contain key regulatory controls involved in development

Answer: Conserved noncoding elements play a fundamental role in regulating animal development
Exact answer: Development
Question: What is the function of mTOR?

Context:
Protein synthesis regulation via mammalian target of rapamycin complex 1 (mTORC1) signaling pathway has key roles in neural development and function,
mTOR regulates assembly of the translation initiation machinery by interacting with the eukaryotic initiation factor eIF3 complex and by controlling phosphorylation of key translational regulators
Mammalian target of rapamycin (mTOR) complexes, mTORC1 and mTORC2, are master regulators of cellular survival, growth and metabolism
 (mTOR) is a serine-threonine kinase that controls several important aspects of mammalian cell function. mTOR activity is modulated by various intra- and extracellular factors; in turn, mTOR changes rates of translation, transcription, protein degradation, cell signaling, metabolism, and cytoskeleton dynamics. mTOR has been repeatedly shown to participate in neuronal development and the proper functioning of mature neurons.
mammalian target of rapamycin (mTOR), a member of the phosphoinositide 3-kinase related kinase (PIKK) family, plays a central role in the regulation of cell growth
(mTOR) is a serine/threonine kinase and that forms two multiprotein complexes known as the mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). mTOR regulates cell growth, proliferation and survival
(mTOR), a downstream effector of the phosphatidylinositol 3-kinase (PI3K)/Akt (protein kinase B) signaling pathway that mediates cell survival and proliferation,

Answer: The mTOR protein regulates assembly of the translation initiation machinery and are master regulators of cellular survival, growth and metabolism.
Question: What is LedPred?

Context:
LedPred: an R/bioconductor package to predict regulatory sequences using support vector machines
Here, we present LedPred, a flexible SVM workflow that predicts new regulatory sequences based on the annotation of known CRMs, which are associated to a large variety of feature types. LedPred is provided as an R/Bioconductor package connected to an online server to avoid installation of non-R software. Due to the heterogeneous CRM feature integration, LedPred excels at the prediction of regulatory sequences in Drosophila and mouse datasets compared with similar SVM-based software.
LedPred: an R/bioconductor package to predict regulatory sequences using support vector machines.
Due to the heterogeneous CRM feature integration, LedPred excels at the prediction of regulatory sequences in Drosophila and mouse datasets compared with similar SVM-based software.
Here, we present LedPred, a flexible SVM workflow that predicts new regulatory sequences based on the annotation of known CRMs, which are associated to a large variety of feature types.
Due to the heterogeneous CRM feature integration, LedPred excels at the prediction of regulatory sequences in Drosophila and mouse datasets compared with similar SVM-based software.LedPred is available on GitHub: https://github.com/aitgon/LedPred and Bioconductor: http://bioconductor.org/packages/release/bioc/html/LedPred.html under the MIT license.aitor.gonzalez@univ-amu.frSupplementary data are available at Bioinformatics online.<CopyrightInformation>© The Author 2015.
LedPred: an R/bioconductor package to predict regulatory sequences using support vector machines.
Due to the heterogeneous CRM feature integration, LedPred excels at the prediction of regulatory sequences in Drosophila and mouse datasets compared with similar SVM-based software.
Here, we present LedPred, a flexible SVM workflow that predicts new regulatory sequences based on the annotation of known CRMs, which are associated to a large variety of feature types.

Answer: LedPred is an R/bioconductor package to predict regulatory sequences using support vector machines. LedPred is provided as an R/Bioconductor package connected to an online server to avoid installation of non-R software. Due to the heterogeneous CRM feature integration, LedPred excels at the prediction of regulatory sequences in Drosophila and mouse datasets compared with similar SVM-based software.
Question: What is the role of AMPK kinase in myocardial remodeling after myocardial infarction

Context:
These data suggest that adiponectin protects the heart from ischemia-reperfusion injury through both AMPK- and COX-2-dependent mechanisms.
The improved cardiac function was associated with decreased atrial natriuretic peptide mRNA levels in the metformin-treated group (50% reduction compared with MI, P < 0.05).
Molecular analyses suggested that altered AMP kinase phosphorylation status and low insulin levels mediate the salutary effects of metformin.
AMP-activated protein kinase (AMPK) is a key sensor of cellular energy. The activation of AMPK by metformin prevents cardiac remodeling after myocardial infarction (MI).
These results suggest that AMPK activation by metformin and the subsequent suppression of TLRs activity could be considered as a target in protecting the infarcted heart, which may indicate a link between AMPK and TLRs.

Answer: AMP-activated protein kinase (AMPK) is a key sensor of cellular energy. The activation of AMPK by metformin prevents cardiac remodeling after myocardial infarction (MI). 
Adiponectin protects the heart from ischemia-reperfusion injury through an AMPK-dependent mechanism.
AMPK activation by metformin and the subsequent suppression of TLRs activity could be considered as a target in protecting the infarcted heart.
Question: In which phase of cell cycle does  stress-induced transcription-associated mutagenesis (TAM) occur?

Context:
factors involved in RNA polymerase (RNAP) processivity or transcriptional derepression contribute to the generation of stress-induced mutations. In Bacillus subtilis, transcription-associated mutagenesis has been shown to be independent of recombination-dependent repair and, in some cases, of the Y DNA polymerases. Central to stationary-phase mutagenesis in B. subtilis is the requirement for Mfd, transcription coupling repair factor
Adaptive (stationary phase) mutagenesis is a phenomenon by which nondividing cells acquire beneficial mutations as a response to stress.
the level of Leu(+) reversions increased significantly in parallel with the induced increase in transcription levels. This mutagenic response was not observed under conditions of exponential growth. Since transcription is a ubiquitous biological process, transcription-associated mutagenesis may influence evolutionary processes in all organisms.
Transcription-associated mutation in Bacillus subtilis cells under stress.
Transcription-associated mutagenesis is increased under stress and depends on the DNA sequence.
Nonrandom transcription-associated mutagenesis under stress should improve the survival of E.
Transcription-associated mutagenesis is increased under stress and depends on the DNA sequence.
Stress-induced mutagenesis describes the accumulation of mutations that occur in nongrowing cells, in contrast to mutagenesis that occurs in actively dividing populations, and has been referred to as stationary-phase or adaptive mutagenesis.
Central to stationary-phase mutagenesis in B

Answer: Factors involved in RNA polymerase (RNAP) processivity or transcriptional derepression, such as Mfd (transcription coupling repair factor), contribute to the generation of stress-induced mutations. Under stress, transcription-associated mutagenesis is increased. Stress-induced transcription-associated mutations are acquired by nondividing cells, during stationary phase, and are not observed under conditions of exponential growth.
Exact answer: stationary phase
Question: What are the birth defects associated with Zika-virus infection?

Context:
the first time after the discovery of ZIKV, the Brazilian scientists are studying the possibility for the virus to cause severe congenital infection related to microcephaly and serious birth defects due to the time-spatial coincidence of the alarming increase of newborns with microcephaly and the Brazilian ZIKV epidemic.
 Although a causal relationship between Zika infection during pregnancy and microcephaly is strongly suspected, such a connection has not yet been scientifically proven. 
a convincing association between Zika virus infection during pregnancy and birth defects, like microcephaly, among some of the newborns.
counseling pregnant women on the risks of fetal microcephaly and other birth defects
evidence suggests that congenital Zika virus infection is associated with microcephaly and other adverse pregnancy and infant outcomes.
the virus has been linked to congenital malformations, including microcephaly and other severe neurological diseases, such as Guillain-Barré syndrome. 
 severe birth defects, such as microcephaly, have been linked to infection during early pregnancy.
n can be prenatally passed from a pregnant woman to her fetus. There is sufficient evidence to conclude that intrauterine Zika virus infection is a cause of microcephaly and serious brain anomalies, but the full spectrum of anomalies has not been delineated. 
Although the full spectrum of adverse reproductive outcomes caused by Zika virus infection is not yet determined, a distinctive phenotype-the congenital Zika syndrome-has emerged.
The current Zika virus (ZIKV) outbreak is associated with high numbers of human congenital birth defects
However, ZIKV infection in early pregnancy has been associated with severe birth defects, including microcephaly and other developmental issues. 
Zika virus (ZIKV) infection is a new emerging threat around the globe which might be responsible for microcephaly and Guillain-Barre syndrome in the infants. 
Zika virus infection during pregnancy is a cause of microcephaly and other severe birth defects 

Answer: Although the full spectrum of adverse reproductive outcomes caused by Zika virus infection is not yet determined, a distinctive phenotype-the congenital Zika syndrome-has emerged. Zika virus infection during pregnancy is a cause of microcephaly and other severe birth defects.
Question: What are the generic versions of Viagra?

Context:
The authors conducted a 12-week case series to study the efficacy and safety of Elonza (generic sildenafil) in PAH patients.

Answer: Generic versions of sildenafil are Elonza, Caverta, Zenegra-100, Vega Asia, Suhagra-100, Vega, Revatio.
Exact answer: Elonza, Caverta, Zenegra-100, Vega Asia, Suhagra-100, Vega
Question: What is the mode of inheritance of Marchesani syndrome?

Context:
Autosomal recessive and autosomal dominant WMS cannot be distinguished by clinical findings alone. 
Weill-Marchesani syndrome (WMS) is a well-characterized disorder in which patients develop eye and skeletal abnormalities. Autosomal-recessive and autosomal-dominant forms of WMS are caused by mutations in ADAMTS10 and FBN1 genes, respectively. 
Finally, WMS is transmitted either by an autosomal dominant or an autosomal recessive (AR) mode of inheritance, GD by an autosomal recessive mode of inheritance and AD by an autosomal dominant mode of inheritance. 
Weill-Marchesani syndrome (WMS) is a rare condition characterized by short stature, brachydactyly, joint stiffness, and characteristic eye abnormalities including microspherophakia, ectopia of lens, severe myopia, and glaucoma. Both autosomal recessive (AR) and autosomal dominant (AD) modes of inheritance have been described for WMS.
Weill-Marchesani syndrome (WMS) is a connective tissue disorder characterised by short stature, brachydactyly, joint stiffness, and characteristic eye anomalies including microspherophakia, ectopia of the lenses, severe myopia, and glaucoma. Both autosomal recessive (AR) and autosomal dominant (AD) modes of inheritance have been described and a gene for AR WMS has recently been mapped to chromosome 19p13.3-p13.2.
Both autosomal recessive and autosomal dominant modes of inheritance have been described in association with WMS. 
We report 6 patients with Weill-Marchesani syndrome (with or without ocular involvement) in three generations, identified by screening 26 members of two families. This is the largest family in the literature showing an autosomal dominant pattern of inheritance.
Weill-Marchesani syndrome comprises short stature, brachydactyly, microspherophakia, glaucoma, and ectopia lentis is regarded as an autosomal recessive trait
We present two families each with affected individuals in 3 generations demonstrating autosomal dominant inheritance of Weill-Marchesani syndrome.
Weill-Marchesani syndrome is a rare, generalized disorder of connective tissue manifested by short stature, brachymorphia, and spherophakia. Inheritance is autosomal recessive.

Answer: Marchesani syndrome is transmitted either by an autosomal dominant (mutations in FBN1) or an autosomal recessive (mutations in ADAMTS10) mode of inheritance
Exact answer: autosomal dominant or autosomal recessive