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SMC5/6 facilitates joint molecule resolution and stepwise loss of cohesin to promote meiotic chromosome segregation

ABSTRACT: During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Diminished Smc5/6 function causes severe defects in nuclear division, but the underlying causes of these defects remain unclear. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of joint-molecule intermediates. Furthermore, we find that Smc5/6 specifically promotes resolution of joint molecules via the XPF-family endonuclease, Mus81-Mms4Eme1. We propose that Smc5/6 acts as a chaperone for ‘mitotic’-like recombination processes during meiosis.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE44852 | GEO | 2013/12/27

SECONDARY ACCESSION(S): PRJNA192193

REPOSITORIES: GEO

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SMC5/6 facilitates joint molecule resolution and stepwise loss of cohesin to promote meiotic chromosome segregation

Project description:During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Diminished Smc5/6 function causes severe defects in nuclear division, but the underlying causes of these defects remain unclear. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of joint-molecule intermediates. Furthermore, we find that Smc5/6 specifically promotes resolution of joint molecules via the XPF-family endonuclease, Mus81-Mms4Eme1. We propose that Smc5/6 acts as a chaperone for M-bM-^@M-^XmitoticM-bM-^@M-^Y-like recombination processes during meiosis. ChIP-chip was used to compare Smc5 localization in wild-type and spo11 strains

2013-12-27 | E-GEOD-44852 | biostudies-arrayexpress

Sister chromatid cohesion halts DNA loop expansion

Project description:Eukaryotic genomes are folded into DNA loops mediated by SMC complexes, like cohesin, condensin and Smc5/6. This organization regulates different DNA related processes along the cell cycle such as transcription, recombination, segregation and DNA repair. During G2/M phases, SMC complexes mediated DNA loops coexist with cohesin complexes involved in sister chromatid cohesion (SCC). It remains unknown whether SCC and DNA loop expansion influence each other and if they cooperate to regulate DNA-related processes. Here we show that SCC is indeed a barrier to DNA loop expansion mediated by cohesin in G2.

2024-01-30 | GSE237031 | GEO

SMC Complexes Are Guarded by the SUMO Protease Ulp2 Against SUMO-Chain-Mediated Turnover

Project description:Structural maintenance of chromosomes (SMC) complexes, cohesin, condensin and Smc5/6, are essential for viability and participate in multiple processes, including sister chromatid cohesion, chromosome condensation, and DNA repair. Here we show that SUMO chains target all three SMC complexes and are antagonized by the SUMO protease Ulp2 to prevent their turnover. We uncover that the essential role of the cohesin-associated subunit Pds5 is to counteract SUMO chains jointly with Ulp2. Importantly, fusion of Ulp2 to kleisin Scc1 supports viability of PDS5 null cells and protects cohesin from proteasomal degradation mediated by the SUMO-targeted ubiquitin ligase Slx5/Slx8. The lethality of PDS5 deleted cells can also be bypassed by simultaneous loss of the PCNA unloader, Elg1, and the cohesin releaser, Wpl1, but only when Ulp2 is functional. Condensin and Smc5/6 complex are similarly guarded by Ulp2 against unscheduled SUMO-chain assembly, which we propose to time the availability of SMC complexes on chromatin.

2021-08-05 | PXD022717 | Pride

Dbf4-dependent kinase (DDK) and the Rtt107 scaffold promote Mus81-Mms4 resolvase activation during mitosis

Project description:DNA repair by homologous recombination is under stringent cell cycle control. This includes the last step of the reaction, disentanglement of DNA joint molecules (JMs). Previous work has established that JMs resolving nucleases are activated specifically at the onset of mitosis. In case of budding yeast Mus81-Mms4, this cell cycle stage-specific activation is known to depend on phosphorylation by CDK and Cdc5 kinases. Here, we show that a third cell cycle kinase, Cdc7-Dbf4 (DDK), targets Mus81-Mms4 in conjunction with Cdc5 - both kinases bind to as well as phosphorylate Mus81-Mms4 in an interdependent manner. Moreover, DDK-mediated phosphorylation of Mms4 is strictly required for Mus81 activation in mitosis, establishing DDK as a novel regulator of homologous recombination. The scaffold protein Rtt107, which is part of the Mus81-Mms4 complex, interacts with Cdc7 and thereby targets DDK and Cdc5 to the complex enabling full Mus81 activation. Therefore, Mus81 activation in mitosis involves at least three cell cycle kinases, Cdk1, Cdc5 and DDK. Furthermore, tethering of the kinases in a stable complex with Mus81 is critical for efficient JM resolution

2017-01-21 | PXD005356 | Pride

Loop-extruding Smc5/6 organizes transcription-induced positive DNA supercoils [ChIP-seq]

Project description:The Structural Maintenance of Chromosome (SMC) protein complexes cohesin, condensin and the Smc5/6 complex (Smc5/6) are essential for chromosome function. At the molecular level, these complexes fold DNA by loop extrusion. Accordingly, cohesin creates chromosome loops in interphase, and condensin compacts mitotic chromosomes. However, the role of Smc5/6’s recently discovered DNA loop extrusion activity is unknown. Here, we uncover that Smc5/6 controls the spatial organization of supercoiled chromosomal regions. The results show that Smc5/6 associates with transcription-induced positively supercoiled chromosomal DNA at cohesin-dependent chromosome loop boundaries. Mechanistically, single-molecule imaging reveals that dimers of Smc5/6 specifically recognize the tip of positively supercoiled DNA plectonemes, and efficiently initiates loop extrusion to gather the supercoiled DNA into a large plectonemic loop. Finally, Hi-C analysis shows that Smc5/6 links chromosomal regions containing transcription-induced positive supercoiling in cis. Altogether, our findings indicate that Smc5/6 controls the three-dimensional organization of chromosomes by recognizing and initiating loop extrusion on positively supercoiled DNA.

2024-01-30 | GSE235557 | GEO

Loop-extruding Smc5/6 organizes transcription-induced positive DNA supercoils [RNA-seq]

2024-01-30 | GSE235559 | GEO

Loop-extruding Smc5/6 organizes transcription-induced positive DNA supercoils [Hi-C]

2024-01-30 | GSE235558 | GEO

Smc5/6-Mms21 prevents and eliminates inappropriate recombination intermediates in meiosis

Project description:Repairing broken chromosomes via joint molecule (JM) intermediates is hazardous and therefore strictly controlled in most organisms. Also in budding yeast meiosis, where production of enough crossovers via JMs is imperative, only a subset of DNA breaks are repaired via JMs, closely regulated by the ZMM pathway. The other breaks are repaired to non-crossovers avoiding JM formation requiring BLM/Sgs1 helicase. "Rogue" JMs that escaped the ZMM pathway and BLM/Sgs1 are eliminated before metaphase by resolvases like Mus81-Mms4 to prevent chromosome nondisjunction. 7 genome-wide meiotic ChIP-seq sets: 2 meiotic time points Smc6-myc DNA interaction (Smc6-ChIP), 2 meiotic time points Smc6-myc DNA interaction in the absence of induced recombination (Smc6-ChIP, spo11delta), 2 meiotic time points Sgs1-myc DNA interaction (Sgs1-ChIP), and 1 meiotic time point untagged as a negative control. (Corresponds to the main Figures 2 and 6, as well as to Figures S4, S7, in the associated publication.)

2013-12-27 | E-GEOD-51977 | biostudies-arrayexpress

Smc5/6 functions with Sgs1-Top3-Rmi1 to complete chromosome replication at natural pause sites

Project description:Smc5/6 is essential for genome structural integrity by yet unknown mechanisms. Here we find that Smc5/6 co-localizes with the DNA crossed-strand processing complex Sgs1-Top3-Rmi1 (STR) at genomic regions known as natural pausing sites (NPSs) where it facilitates Top3 retention. Individual depletions of STR subunits and Smc5/6 cause similar accumulation of joint molecules (JMs) composed of reversed forks, double Holliday Junctions and hemicatenanes, indicative of Smc5/6 regulating Sgs1 and Top3 DNA processing activities. We isolate an intra-allelic suppressor of smc6-56 proficient in Top3 retention but affected in pathways that act complementarily with Sgs1 and Top3 to resolve JMs arising at replication termination. Upon replication stress, the smc6-56 suppressor requires STR and Mus81-Mms4 functions for recovery, but not Srs2 and Mph1 helicases that prevent maturation of recombination intermediates. Thus, Smc5/6 functions jointly with Top3 and STR to mediate replication completion and influences the function of other DNA crossed-strand processing enzymes at NPSs.

2021-02-03 | GSE147452 | GEO

Functional characterization of NSE4A subunit of SMC5/6 complex in Arabidopsis

Project description:The control of genome integrity throughout cellular generations is critical for plant development and the correct transmission of genetic information to the progeny. A key factor involved in this process is STRUCTURAL MAINTAINANCE OF CHROMOSOME 5/6 (SMC5/6) complex, related to cohesin and condensin complexes. Here, we analyzed mRNA abundance changes in the partial loss of function mutant of NON-SMC ELEMENT 4A (nse4a-2 mutant allele), a subunit of SMC5/6 complex, in Arabidopsis.

2018-06-06 | GSE113310 | GEO

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