SLY regulates genes involved in chromatin remodeling and interacts with TBL1XR1 during sperm differentiation.
Identifieur interne : 000A47 ( PubMed/Curation ); précédent : 000A46; suivant : 000A48SLY regulates genes involved in chromatin remodeling and interacts with TBL1XR1 during sperm differentiation.
Auteurs : Charlotte Moretti [France] ; Maria-Elisabetta Serrentino [France] ; Côme Ialy-Radio [France] ; Marion Delessard [France] ; Tatiana A. Soboleva [Australie] ; Frederic Tores [France] ; Marjorie Leduc [France] ; Patrick Nitschké [France] ; Joel R. Drevet [France] ; David J. Tremethick [Australie] ; Daniel Vaiman [France] ; Ayhan Kocer [France] ; Julie Cocquet [France]Source :
- Cell death and differentiation [ 1476-5403 ] ; 2017.
Abstract
Sperm differentiation requires unique transcriptional regulation and chromatin remodeling after meiosis to ensure proper compaction and protection of the paternal genome. Abnormal sperm chromatin remodeling can induce sperm DNA damage, embryo lethality and male infertility, yet, little is known about the factors which regulate this process. Deficiency in Sly, a mouse Y chromosome-encoded gene expressed only in postmeiotic male germ cells, has been shown to result in the deregulation of hundreds of sex chromosome-encoded genes associated with multiple sperm differentiation defects and subsequent male infertility. The underlying mechanism remained, to date, unknown. Here, we show that SLY binds to the promoter of sex chromosome-encoded and autosomal genes highly expressed postmeiotically and involved in chromatin regulation. Specifically, we demonstrate that Sly knockdown directly induces the deregulation of sex chromosome-encoded H2A variants and of the H3K79 methyltransferase DOT1L. The modifications prompted by loss of Sly alter the postmeiotic chromatin structure and ultimately result in abnormal sperm chromatin remodeling with negative consequences on the sperm genome integrity. Altogether our results show that SLY is a regulator of sperm chromatin remodeling. Finally we identified that SMRT/N-CoR repressor complex is involved in gene regulation during sperm differentiation since members of this complex, in particular TBL1XR1, interact with SLY in postmeiotic male germ cells.
DOI: 10.1038/cdd.2017.32
PubMed: 28475176
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Soboleva</name><affiliation wicri:level="1"><nlm:affiliation>The John Curtin School of Medical Research, The Australian National University, PO Box 334, Canberra, ACT 2601, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The John Curtin School of Medical Research, The Australian National University, PO Box 334, Canberra, ACT 2601</wicri:regionArea></affiliation></author><author><name sortKey="Tores, Frederic" sort="Tores, Frederic" uniqKey="Tores F" first="Frederic" last="Tores">Frederic Tores</name><affiliation wicri:level="1"><nlm:affiliation>Bioinformatics facility, Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Bioinformatics facility, Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Leduc, Marjorie" sort="Leduc, Marjorie" uniqKey="Leduc M" first="Marjorie" last="Leduc">Marjorie Leduc</name><affiliation wicri:level="1"><nlm:affiliation>3P5 proteomic facility, Institut Cochin, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>3P5 proteomic facility, Institut Cochin, Université Paris Descartes, Sorbonne Paris Cité, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Nitschke, Patrick" sort="Nitschke, Patrick" uniqKey="Nitschke P" first="Patrick" last="Nitschké">Patrick Nitschké</name><affiliation wicri:level="1"><nlm:affiliation>Bioinformatics facility, Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Bioinformatics facility, Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Drevet, Joel R" sort="Drevet, Joel R" uniqKey="Drevet J" first="Joel R" last="Drevet">Joel R. Drevet</name><affiliation wicri:level="1"><nlm:affiliation>Genetic Reproduction and Development, CNRS UMR6293 - INSERM U1103 - Clermont Université, 63178 Aubière Cedex, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Genetic Reproduction and Development, CNRS UMR6293 - INSERM U1103 - Clermont Université, 63178 Aubière Cedex</wicri:regionArea></affiliation></author><author><name sortKey="Tremethick, David J" sort="Tremethick, David J" uniqKey="Tremethick D" first="David J" last="Tremethick">David J. Tremethick</name><affiliation wicri:level="1"><nlm:affiliation>The John Curtin School of Medical Research, The Australian National University, PO Box 334, Canberra, ACT 2601, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>The John Curtin School of Medical Research, The Australian National University, PO Box 334, Canberra, ACT 2601</wicri:regionArea></affiliation></author><author><name sortKey="Vaiman, Daniel" sort="Vaiman, Daniel" uniqKey="Vaiman D" first="Daniel" last="Vaiman">Daniel Vaiman</name><affiliation wicri:level="1"><nlm:affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Kocer, Ayhan" sort="Kocer, Ayhan" uniqKey="Kocer A" first="Ayhan" last="Kocer">Ayhan Kocer</name><affiliation wicri:level="1"><nlm:affiliation>Genetic Reproduction and Development, CNRS UMR6293 - INSERM U1103 - Clermont Université, 63178 Aubière Cedex, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Genetic Reproduction and Development, CNRS UMR6293 - INSERM U1103 - Clermont Université, 63178 Aubière Cedex</wicri:regionArea></affiliation></author><author><name sortKey="Cocquet, Julie" sort="Cocquet, Julie" uniqKey="Cocquet J" first="Julie" last="Cocquet">Julie Cocquet</name><affiliation wicri:level="1"><nlm:affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cell death and differentiation</title><idno type="eISSN">1476-5403</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sperm differentiation requires unique transcriptional regulation and chromatin remodeling after meiosis to ensure proper compaction and protection of the paternal genome. Abnormal sperm chromatin remodeling can induce sperm DNA damage, embryo lethality and male infertility, yet, little is known about the factors which regulate this process. Deficiency in Sly, a mouse Y chromosome-encoded gene expressed only in postmeiotic male germ cells, has been shown to result in the deregulation of hundreds of sex chromosome-encoded genes associated with multiple sperm differentiation defects and subsequent male infertility. The underlying mechanism remained, to date, unknown. Here, we show that SLY binds to the promoter of sex chromosome-encoded and autosomal genes highly expressed postmeiotically and involved in chromatin regulation. Specifically, we demonstrate that Sly knockdown directly induces the deregulation of sex chromosome-encoded H2A variants and of the H3K79 methyltransferase DOT1L. The modifications prompted by loss of Sly alter the postmeiotic chromatin structure and ultimately result in abnormal sperm chromatin remodeling with negative consequences on the sperm genome integrity. Altogether our results show that SLY is a regulator of sperm chromatin remodeling. Finally we identified that SMRT/N-CoR repressor complex is involved in gene regulation during sperm differentiation since members of this complex, in particular TBL1XR1, interact with SLY in postmeiotic male germ cells.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">28475176</PMID><DateCreated><Year>2017</Year><Month>05</Month><Day>05</Day></DateCreated><DateRevised><Year>2017</Year><Month>06</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5403</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>6</Issue><PubDate><Year>2017</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Cell death and differentiation</Title><ISOAbbreviation>Cell Death Differ.</ISOAbbreviation></Journal><ArticleTitle>SLY regulates genes involved in chromatin remodeling and interacts with TBL1XR1 during sperm differentiation.</ArticleTitle><Pagination><MedlinePgn>1029-1044</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/cdd.2017.32</ELocationID><Abstract><AbstractText>Sperm differentiation requires unique transcriptional regulation and chromatin remodeling after meiosis to ensure proper compaction and protection of the paternal genome. Abnormal sperm chromatin remodeling can induce sperm DNA damage, embryo lethality and male infertility, yet, little is known about the factors which regulate this process. Deficiency in Sly, a mouse Y chromosome-encoded gene expressed only in postmeiotic male germ cells, has been shown to result in the deregulation of hundreds of sex chromosome-encoded genes associated with multiple sperm differentiation defects and subsequent male infertility. The underlying mechanism remained, to date, unknown. Here, we show that SLY binds to the promoter of sex chromosome-encoded and autosomal genes highly expressed postmeiotically and involved in chromatin regulation. Specifically, we demonstrate that Sly knockdown directly induces the deregulation of sex chromosome-encoded H2A variants and of the H3K79 methyltransferase DOT1L. The modifications prompted by loss of Sly alter the postmeiotic chromatin structure and ultimately result in abnormal sperm chromatin remodeling with negative consequences on the sperm genome integrity. Altogether our results show that SLY is a regulator of sperm chromatin remodeling. Finally we identified that SMRT/N-CoR repressor complex is involved in gene regulation during sperm differentiation since members of this complex, in particular TBL1XR1, interact with SLY in postmeiotic male germ cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Moretti</LastName><ForeName>Charlotte</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, UMR8104, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Serrentino</LastName><ForeName>Maria-Elisabetta</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, UMR8104, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ialy-Radio</LastName><ForeName>Côme</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, UMR8104, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delessard</LastName><ForeName>Marion</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, UMR8104, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Soboleva</LastName><ForeName>Tatiana A</ForeName><Initials>TA</Initials><AffiliationInfo><Affiliation>The John Curtin School of Medical Research, The Australian National University, PO Box 334, Canberra, ACT 2601, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tores</LastName><ForeName>Frederic</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Bioinformatics facility, Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leduc</LastName><ForeName>Marjorie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>3P5 proteomic facility, Institut Cochin, Université Paris Descartes, Sorbonne Paris Cité, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nitschké</LastName><ForeName>Patrick</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Bioinformatics facility, Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drevet</LastName><ForeName>Joel R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Genetic Reproduction and Development, CNRS UMR6293 - INSERM U1103 - Clermont Université, 63178 Aubière Cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tremethick</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>The John Curtin School of Medical Research, The Australian National University, PO Box 334, Canberra, ACT 2601, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vaiman</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-1915-0717</Identifier><AffiliationInfo><Affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, UMR8104, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kocer</LastName><ForeName>Ayhan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Genetic Reproduction and Development, CNRS UMR6293 - INSERM U1103 - Clermont Université, 63178 Aubière Cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cocquet</LastName><ForeName>Julie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Development, Reproduction and Cancer, INSERM, U1016, Institut Cochin, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, UMR8104, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, Paris, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>05</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Death Differ</MedlineTA><NlmUniqueID>9437445</NlmUniqueID><ISSNLinking>1350-9047</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cold 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