Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pgen.1003985
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dc.titleMeiotic Cohesin SMCβ Provides Prophase I Centromeric Cohesion and Is Required for Multiple Synapsis-Associated Functions
dc.contributor.authorBiswas U.
dc.contributor.authorWetzker C.
dc.contributor.authorLange J.
dc.contributor.authorChristodoulou E.G.
dc.contributor.authorSeifert M.
dc.contributor.authorBeyer A.
dc.contributor.authorJessberger R.
dc.date.accessioned2020-03-13T05:25:15Z
dc.date.available2020-03-13T05:25:15Z
dc.date.issued2013
dc.identifier.citationBiswas U., Wetzker C., Lange J., Christodoulou E.G., Seifert M., Beyer A., Jessberger R. (2013). Meiotic Cohesin SMCβ Provides Prophase I Centromeric Cohesion and Is Required for Multiple Synapsis-Associated Functions. PLoS Genetics 9 (12) : e1003985. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pgen.1003985
dc.identifier.issn15537390
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/165400
dc.description.abstractCohesin subunit SMC1β is specific and essential for meiosis. Previous studies showed functions of SMC1β in determining the axis-loop structure of synaptonemal complexes (SCs), in providing sister chromatid cohesion (SCC) in metaphase I and thereafter, in protecting telomere structure, and in synapsis. However, several central questions remained unanswered and concern roles of SMC1β in SCC and synapsis and processes related to these two processes. Here we show that SMC1β substantially supports prophase I SCC at centromeres but not along chromosome arms. Arm cohesion and some of centromeric cohesion in prophase I are provided by non-phosphorylated SMC1α. Besides supporting synapsis of autosomes, SMC1β is also required for synapsis and silencing of sex chromosomes. In absence of SMC1β, the silencing factor γH2AX remains associated with asynapsed autosomes and fails to localize to sex chromosomes. Microarray expression studies revealed up-regulated sex chromosome genes and many down-regulated autosomal genes. SMC1β is further required for non-homologous chromosome associations observed in absence of SPO11 and thus of programmed double-strand breaks. These breaks are properly generated in Smc1β-/- spermatocytes, but their repair is delayed on asynapsed chromosomes. SMC1α alone cannot support non-homologous associations. Together with previous knowledge, three main functions of SMC1β have emerged, which have multiple consequences for spermatocyte biology: generation of the loop-axis architecture of SCs, homologous and non-homologous synapsis, and SCC starting in early prophase I. © 2013 Biswas et al.
dc.publisherPublic Library of Science
dc.sourceUnpaywall 20200320
dc.subjectcell protein
dc.subjectcohesin
dc.subjectprotein gamma H2AX
dc.subjectprotein SMC1 alpha
dc.subjectprotein SMC1 beta
dc.subjectSpo11 protein
dc.subjectunclassified drug
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectarticle
dc.subjectautosome
dc.subjectcell adhesion
dc.subjectcentromere
dc.subjectchromosome pairing
dc.subjectcontrolled study
dc.subjectdouble stranded DNA break
dc.subjectdown regulation
dc.subjectgene expression regulation
dc.subjectgene location
dc.subjectgene silencing
dc.subjectmale
dc.subjectmeiotic prophase I
dc.subjectmicroarray analysis
dc.subjectmouse
dc.subjectnonhuman
dc.subjectprotein function
dc.subjectsex linkage
dc.subjectsister chromatid
dc.subjectsister chromatid cohesion
dc.subjectspermatocyte
dc.subjectsynaptonemal complex
dc.subjecttelomere
dc.subjectupregulation
dc.subjectAnimals
dc.subjectCell Cycle Proteins
dc.subjectCentromere
dc.subjectChromosome Pairing
dc.subjectChromosome Segregation
dc.subjectEndodeoxyribonucleases
dc.subjectMale
dc.subjectMeiosis
dc.subjectMeiotic Prophase I
dc.subjectMice
dc.subjectSpermatocytes
dc.subjectSynaptonemal Complex
dc.subjectTelomere
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1371/journal.pgen.1003985
dc.description.sourcetitlePLoS Genetics
dc.description.volume9
dc.description.issue12
dc.description.pagee1003985
dc.published.statePublished
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