fhl1 gene of the fission yeast regulates transcription of meiotic genes and nitrogen starvation response, downstream of the TORC1 pathway.
Identifieur interne : 000690 ( Main/Exploration ); précédent : 000689; suivant : 000691fhl1 gene of the fission yeast regulates transcription of meiotic genes and nitrogen starvation response, downstream of the TORC1 pathway.
Auteurs : Emese Pataki [Hongrie] ; Ronit Weisman [Israël] ; Matthias Sipiczki [Hongrie] ; Ida Miklos [Hongrie]Source :
- Current genetics [ 1432-0983 ] ; 2017.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes (MeSH), Analyse de regroupements (MeSH), Annotation de séquence moléculaire (MeSH), Azote (métabolisme), Biologie informatique (méthodes), Complexe-1 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (métabolisme), Facteurs de transcription Forkhead (génétique), Mutation (MeSH), Méiose (génétique), Protéines de Schizosaccharomyces pombe (génétique), Régions promotrices (génétique) (MeSH), Régulation de l'expression des gènes fongiques (MeSH), Schizosaccharomyces (génétique), Schizosaccharomyces (métabolisme), Spores fongiques (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH), Étude d'association pangénomique (MeSH).
- MESH :
- génétique : Facteurs de transcription Forkhead, Méiose, Protéines de Schizosaccharomyces pombe, Schizosaccharomyces, Spores fongiques.
- métabolisme : Azote, Complexes multiprotéiques, Schizosaccharomyces, Sérine-thréonine kinases TOR.
- méthodes : Biologie informatique.
- Analyse de profil d'expression de gènes, Analyse de regroupements, Annotation de séquence moléculaire, Complexe-1 cible mécanistique de la rapamycine, Mutation, Régions promotrices (génétique), Régulation de l'expression des gènes fongiques, Transduction du signal, Étude d'association pangénomique.
English descriptors
- KwdEn :
- Cluster Analysis (MeSH), Computational Biology (methods), Forkhead Transcription Factors (genetics), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (MeSH), Genome-Wide Association Study (MeSH), Mechanistic Target of Rapamycin Complex 1 (MeSH), Meiosis (genetics), Molecular Sequence Annotation (MeSH), Multiprotein Complexes (metabolism), Mutation (MeSH), Nitrogen (metabolism), Promoter Regions, Genetic (MeSH), Schizosaccharomyces (genetics), Schizosaccharomyces (metabolism), Schizosaccharomyces pombe Proteins (genetics), Signal Transduction (MeSH), Spores, Fungal (genetics), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , genetics : Forkhead Transcription Factors, Schizosaccharomyces pombe Proteins.
- genetics : Meiosis, Schizosaccharomyces, Spores, Fungal.
- chemical , metabolism : Multiprotein Complexes, Nitrogen, Schizosaccharomyces, TOR Serine-Threonine Kinases.
- methods : Computational Biology.
- Cluster Analysis, Gene Expression Profiling, Gene Expression Regulation, Fungal, Genome-Wide Association Study, Mechanistic Target of Rapamycin Complex 1, Molecular Sequence Annotation, Mutation, Promoter Regions, Genetic, Signal Transduction.
Abstract
Environmental changes, such as nutrient limitation or starvation induce different signal transducing pathways, which require coordinated cooperation of several genes. Our previous data revealed that the fhl1 fork-head type transcription factor of the fission yeast could be involved in sporulation, which was typically induced under poor conditions. Since the exact role of Fhl1 in this process was not known, we wanted to identify its downstream targets and to investigate its possible cooperation with another known regulator of sporulation. Gene expression and Northern blot analysis of the fhl1∆ mutant strain revealed the target genes involved in mating and sporulation. Our results also showed that Fhl1 could regulate nutrient sensing, the transporter and permease genes. Since the majority of these genes belonged to the nitrogen starvation response, the possible cooperation of fhl1 and tor2 was also investigated. Comparison of their microarray data and the expression of fhl1 + from a strong promoter in the tor2-ts mutant cells suggested that one part of the target genes are commonly regulated by Fhl1 and Tor2. Since the expression of fhl1 + from a strong promoter could rescue rapamycin and temperature sensitivity and suppressed the hyper-sporulation defect of the tor2-ts mutant cells, we believe that Fhl1 acts in TOR signaling, downstream of Tor2. Thus, this work shed light on certain novel details of the regulation of the sexual processes and a new member of the TOR pathway, but further experiments are needed to confirm the involvement of Fhl1 in nutrient sensing.
DOI: 10.1007/s00294-016-0607-1
PubMed: 27165118
Affiliations:
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promotrices (génétique)</term><term>Régulation de l'expression des gènes fongiques</term><term>Transduction du signal</term><term>Étude d'association pangénomique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Environmental changes, such as nutrient limitation or starvation induce different signal transducing pathways, which require coordinated cooperation of several genes. Our previous data revealed that the fhl1 fork-head type transcription factor of the fission yeast could be involved in sporulation, which was typically induced under poor conditions. Since the exact role of Fhl1 in this process was not known, we wanted to identify its downstream targets and to investigate its possible cooperation with another known regulator of sporulation. Gene expression and Northern blot analysis of the fhl1∆ mutant strain revealed the target genes involved in mating and sporulation. Our results also showed that Fhl1 could regulate nutrient sensing, the transporter and permease genes. Since the majority of these genes belonged to the nitrogen starvation response, the possible cooperation of fhl1 and tor2 was also investigated. Comparison of their microarray data and the expression of fhl1 <sup>+</sup> from a strong promoter in the tor2-ts mutant cells suggested that one part of the target genes are commonly regulated by Fhl1 and Tor2. Since the expression of fhl1 <sup>+</sup> from a strong promoter could rescue rapamycin and temperature sensitivity and suppressed the hyper-sporulation defect of the tor2-ts mutant cells, we believe that Fhl1 acts in TOR signaling, downstream of Tor2. Thus, this work shed light on certain novel details of the regulation of the sexual processes and a new member of the TOR pathway, but further experiments are needed to confirm the involvement of Fhl1 in nutrient sensing.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27165118</PMID><DateCompleted><Year>2017</Year><Month>02</Month><Day>14</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-0983</ISSN><JournalIssue CitedMedium="Internet"><Volume>63</Volume><Issue>1</Issue><PubDate><Year>2017</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Current genetics</Title><ISOAbbreviation>Curr Genet</ISOAbbreviation></Journal><ArticleTitle>fhl1 gene of the fission yeast regulates transcription of meiotic genes and nitrogen starvation response, downstream of the TORC1 pathway.</ArticleTitle><Pagination><MedlinePgn>91-101</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00294-016-0607-1</ELocationID><Abstract><AbstractText>Environmental changes, such as nutrient limitation or starvation induce different signal transducing pathways, which require coordinated cooperation of several genes. Our previous data revealed that the fhl1 fork-head type transcription factor of the fission yeast could be involved in sporulation, which was typically induced under poor conditions. Since the exact role of Fhl1 in this process was not known, we wanted to identify its downstream targets and to investigate its possible cooperation with another known regulator of sporulation. Gene expression and Northern blot analysis of the fhl1∆ mutant strain revealed the target genes involved in mating and sporulation. Our results also showed that Fhl1 could regulate nutrient sensing, the transporter and permease genes. Since the majority of these genes belonged to the nitrogen starvation response, the possible cooperation of fhl1 and tor2 was also investigated. Comparison of their microarray data and the expression of fhl1 <sup>+</sup> from a strong promoter in the tor2-ts mutant cells suggested that one part of the target genes are commonly regulated by Fhl1 and Tor2. Since the expression of fhl1 <sup>+</sup> from a strong promoter could rescue rapamycin and temperature sensitivity and suppressed the hyper-sporulation defect of the tor2-ts mutant cells, we believe that Fhl1 acts in TOR signaling, downstream of Tor2. Thus, this work shed light on certain novel details of the regulation of the sexual processes and a new member of the TOR pathway, but further experiments are needed to confirm the involvement of Fhl1 in nutrient sensing.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pataki</LastName><ForeName>Emese</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Genetics and Applied Microbiology, Faculty of Science and Technology, University of Debrecen, Egyetem tér 1, 4032, Debrecen, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Weisman</LastName><ForeName>Ronit</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Natural and Life Sciences, The Open University of Israel, University Road 1, 4353701, Ranana, Israel.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sipiczki</LastName><ForeName>Matthias</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Genetics and Applied Microbiology, Faculty of Science and Technology, University of Debrecen, Egyetem tér 1, 4032, Debrecen, Hungary.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miklos</LastName><ForeName>Ida</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Genetics and Applied Microbiology, Faculty of Science and Technology, University of Debrecen, Egyetem tér 1, 4032, Debrecen, Hungary. miklos.ida@science.unideb.hu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Curr Genet</MedlineTA><NlmUniqueID>8004904</NlmUniqueID><ISSNLinking>0172-8083</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C500535">Fhl1 protein, S pombe</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D046912">Multiprotein Complexes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029702">Schizosaccharomyces pombe Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>N762921K75</RegistryNumber><NameOfSubstance UI="D009584">Nitrogen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016000" MajorTopicYN="N">Cluster Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019295" MajorTopicYN="N">Computational Biology</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="Y">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055106" MajorTopicYN="N">Genome-Wide 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Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012568" MajorTopicYN="N">Schizosaccharomyces</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029702" MajorTopicYN="N">Schizosaccharomyces pombe Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013172" MajorTopicYN="N">Spores, Fungal</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Fork-head transcription factor</Keyword><Keyword MajorTopicYN="N">Gene expression analysis</Keyword><Keyword MajorTopicYN="N">Nitrogen response</Keyword><Keyword MajorTopicYN="N">Schizosaccharomyces pombe</Keyword><Keyword MajorTopicYN="N">Sporulation</Keyword><Keyword MajorTopicYN="N">TOR pathway</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>03</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>04</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>04</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>5</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>2</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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