scholarly journals The Cohesin Subunit Rad21 Is Required for Synaptonemal Complex Maintenance, but Not Sister Chromatid Cohesion, during Drosophila Female Meiosis

PLoS Genetics ◽  
2014 ◽  
Vol 10 (8) ◽  
pp. e1004540 ◽  
Author(s):  
Evelin Urban ◽  
Sonal Nagarkar-Jaiswal ◽  
Christian F. Lehner ◽  
Stefan K. Heidmann
2009 ◽  
Vol 20 (3) ◽  
pp. 1030-1047 ◽  
Author(s):  
Gloria A. Brar ◽  
Andreas Hochwagen ◽  
Ly-sha S. Ee ◽  
Angelika Amon

Sister chromatid cohesion, mediated by cohesin complexes, is laid down during DNA replication and is essential for the accurate segregation of chromosomes. Previous studies indicated that, in addition to their cohesion function, cohesins are essential for completion of recombination, pairing, meiotic chromosome axis formation, and assembly of the synaptonemal complex (SC). Using mutants in the cohesin subunit Rec8, in which phosphorylated residues were mutated to alanines, we show that cohesin phosphorylation is not only important for cohesin removal, but that cohesin's meiotic prophase functions are distinct from each other. We find pairing and SC formation to be dependent on Rec8, but independent of the presence of a sister chromatid and hence sister chromatid cohesion. We identified mutations in REC8 that differentially affect Rec8's cohesion, pairing, recombination, chromosome axis and SC assembly function. These findings define Rec8 as a key determinant of meiotic chromosome morphogenesis and a central player in multiple meiotic events.


2011 ◽  
Vol 22 (12) ◽  
pp. 1985-1996 ◽  
Author(s):  
Weiqiang Lin ◽  
Hui Jin ◽  
Xiuwen Liu ◽  
Kristin Hampton ◽  
Hong-Guo Yu

To tether sister chromatids, a protein-loading complex, including Scc2, recruits cohesin to the chromosome at discrete loci. Cohesin facilitates the formation of a higher-order chromosome structure that could also influence gene expression. How cohesin directly regulates transcription remains to be further elucidated. We report that in budding yeast Scc2 is required for sister-chromatid cohesion during meiosis for two reasons. First, Scc2 is required for activating the expression of REC8, which encodes a meiosis-specific cohesin subunit; second, Scc2 is necessary for recruiting meiotic cohesin to the chromosome to generate sister-chromatid cohesion. Using a heterologous reporter assay, we have found that Scc2 increases the activity of its target promoters by recruiting cohesin to establish an upstream cohesin-associated region in a position-dependent manner. Rec8-associated meiotic cohesin is required for the full activation of the REC8 promoter, revealing that cohesin has a positive feedback on transcriptional regulation. Finally, we provide evidence that chromosomal binding of cohesin is sufficient for target-gene activation during meiosis. Our data support a noncanonical role for cohesin as a transcriptional activator during cell differentiation.


2018 ◽  
Vol 29 (3) ◽  
pp. 339-355 ◽  
Author(s):  
Brett Robison ◽  
Vincent Guacci ◽  
Douglas Koshland

A screen of cohesin subunit Smc3 reveals that its hinge is a nexus controlling the maintenance of sister chromatid cohesion and condensation.


2009 ◽  
Vol 186 (5) ◽  
pp. 713-725 ◽  
Author(s):  
Hui Jin ◽  
Vincent Guacci ◽  
Hong-Guo Yu

During meiosis, homologues become juxtaposed and synapsed along their entire length. Mutations in the cohesin complex disrupt not only sister chromatid cohesion but also homologue pairing and synaptonemal complex formation. In this study, we report that Pds5, a cohesin-associated protein known to regulate sister chromatid cohesion, is required for homologue pairing and synapsis in budding yeast. Pds5 colocalizes with cohesin along the length of meiotic chromosomes. In the absence of Pds5, the meiotic cohesin subunit Rec8 remains bound to chromosomes with only minor defects in sister chromatid cohesion, but sister chromatids synapse instead of homologues. Double-strand breaks (DSBs) are formed but are not repaired efficiently. In addition, meiotic chromosomes undergo hypercondensation. When the mitotic cohesin subunit Mcd1 is substituted for Rec8 in Pds5-depleted cells, chromosomes still hypercondense, but synapsis of sister chromatids is abolished. These data suggest that Pds5 modulates the Rec8 activity to facilitate chromosome morphological changes required for homologue synapsis, DSB repair, and meiotic chromosome segregation.


1998 ◽  
Vol 140 (5) ◽  
pp. 1003-1012 ◽  
Author(s):  
Daniel P. Moore ◽  
Andrea W. Page ◽  
Tracy Tzu-Ling Tang ◽  
Anne W. Kerrebrock ◽  
Terry L. Orr-Weaver

The Drosophila MEI-S332 protein has been shown to be required for the maintenance of sister-chromatid cohesion in male and female meiosis. The protein localizes to the centromeres during male meiosis when the sister chromatids are attached, and it is no longer detectable after they separate. Drosophila melanogaster male meiosis is atypical in several respects, making it important to define MEI-S332 behavior during female meiosis, which better typifies meiosis in eukaryotes. We find that MEI-S332 localizes to the centromeres of prometaphase I chromosomes in oocytes, remaining there until it is delocalized at anaphase II. By using oocytes we were able to obtain sufficient material to investigate the fate of MEI-S332 after the metaphase II–anaphase II transition. The levels of MEI-S332 protein are unchanged after the completion of meiosis, even when translation is blocked, suggesting that the protein dissociates from the centromeres but is not degraded at the onset of anaphase II. Unexpectedly, MEI-S332 is present during embryogenesis, localizes onto the centromeres of mitotic chromosomes, and is delocalized from anaphase chromosomes. Thus, MEI-S332 associates with the centromeres of both meiotic and mitotic chromosomes and dissociates from them at anaphase.


2020 ◽  
Vol 3 (3) ◽  
pp. e201900564 ◽  
Author(s):  
François McNicoll ◽  
Anne Kühnel ◽  
Uddipta Biswas ◽  
Kai Hempel ◽  
Gabriela Whelan ◽  
...  

In mitotic cells, establishment of sister chromatid cohesion requires acetylation of the cohesin subunit SMC3 (acSMC3) by ESCO1 and/or ESCO2. Meiotic cohesin plays additional but poorly understood roles in the formation of chromosome axial elements (AEs) and synaptonemal complexes. Here, we show that levels of ESCO2, acSMC3, and the pro-cohesion factor sororin increase on meiotic chromosomes as homologs synapse. These proteins are less abundant on the largely unsynapsed sex chromosomes, whose sister chromatid cohesion appears weaker throughout the meiotic prophase. Using three distinct conditional Esco2 knockout mouse strains, we demonstrate that ESCO2 is essential for male gametogenesis. Partial depletion of ESCO2 in prophase I spermatocytes delays chromosome synapsis and further weakens cohesion along sex chromosomes, which show extensive separation of AEs into single chromatids. Unsynapsed regions of autosomes are associated with the sex chromatin and also display split AEs. This study provides the first evidence for a specific role of ESCO2 in mammalian meiosis, identifies a particular ESCO2 dependence of sex chromosome cohesion and suggests support of autosomal synapsis by acSMC3-stabilized cohesion.


2007 ◽  
Vol 17 (17) ◽  
pp. 1489-1497 ◽  
Author(s):  
Nicolas Malmanche ◽  
Stephanie Owen ◽  
Stephen Gegick ◽  
Soren Steffensen ◽  
John E. Tomkiel ◽  
...  

2019 ◽  
Author(s):  
Atiq Faramarz ◽  
Jesper A. Balk ◽  
Anneke B. Oostra ◽  
Cherien A. Ghandour ◽  
Martin A. Rooimans ◽  
...  

AbstractIn a process linked to DNA replication, duplicated chromosomes are co-entrapped into large, circular cohesin complexes and functional sister chromatid cohesion (SCC) is established by acetylation of the SMC3 cohesin subunit. Several rare human developmental syndromes are characterized by defective SCC. Roberts Syndrome (RBS) is caused by mutations in the SMC3 acetyl transferase ESCO2, whereas mutations in the DNA helicase DDX11 lead to Warsaw Breakage Syndrome (WABS). We found that WABS-derived cells predominantly rely on ESCO2, not ESCO1, for residual SCC, growth and survival. Reciprocally, RBS-derived cells depend on DDX11 to maintain low levels of SCC. Synthetic lethality between DDX11 and ESCO2 correlated with a prolonged delay in mitosis, and was rescued by knock down of the cohesion remover WAPL. Rescue experiments using mouse or human cDNAs revealed that DDX11, ESCO1 and ESCO2 act on differential aspects of DNA replication-coupled SCC establishment. Importantly, DDX11 is required for normal DNA replication fork speed without clearly affecting SMC3 acetylation. We propose that DDX11 and ESCO2 control spatially separated fractions of cohesin, with supportive roles for DDX11 in replication-associated cohesion establishment, and for ESCO2 in cohesin complexes located around centromeres, respectively.


Sign in / Sign up

Export Citation Format

Share Document