Distinct activities of bacterial condensins for chromosome management in Pseudomonas aeruginosa
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ABSTRACT:
PROVIDER: PRJNA633913 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11814600_1.fastq.gz | Fastqsanger.gz | |||
| SRR11814600_2.fastq.gz | Fastqsanger.gz | |||
| SRR11814601_1.fastq.gz | Fastqsanger.gz | |||
| SRR11814601_2.fastq.gz | Fastqsanger.gz | |||
| SRR11814602_1.fastq.gz | Fastqsanger.gz |
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Project description:Three types of structurally related structural maintenance of chromosomes (SMC) complexes, referred to as condensins, have been identified in bacteria. Smc-ScpAB is present in most bacteria, whereas MukBEF is found in enterobacteria and MksBEF is scattered over the phylogenic tree. The contributions of these condensins to chromosome management were characterized in Pseudomonas aeruginosa, which carries both Smc-ScpAB and MksBEF. In this bacterium, SMC-ScpAB controls chromosome disposition by juxtaposing chromosome arms. In contrast, MksBEF is critical for chromosome segregation in the absence of the main segregation system, and it affects the higher-order architecture of the chromosome by promoting DNA contacts in the megabase range. Strikingly, our results reveal a prevalence of Smc-ScpAB over MksBEF involving a coordination of their activities with chromosome replication. They also show that E. coli MukBEF can substitute for MksBEF in P. aeruginosa while prevailing over Smc-ScpAB. Our results reveal a hierarchy between activities of bacterial condensins on the same chromosome.
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Project description:During mitosis, interphase chromatin is rapidly converted into rod-shaped mitotic chromosomes. Using Hi-C, imaging, proteomics and polymer modeling, we determine how the activity and interplay between loop-extruding SMC motors accomplishes this dramatic transition. Our work reveals rules of engagement for SMC complexes that are critical for allowing cells to refold interphase chromatin into mitotic chromosomes. We find that condensin disassembles interphase chromatin loop organization by evicting or displacing extrusive cohesin. In contrast, condensin bypasses cohesive cohesins, thereby maintaining sister chromatid cohesion while separating the sisters. Studies of mitotic chromosomes formed by cohesin, condensin II and condensin I alone or in combination allow us to develop new models of mitotic chromosome conformation. In these models, loops are consecutive and not overlapping, implying that condensins do not freely pass one another but stall upon encountering each other. The dynamics of Hi-C interactions and chromosome morphology reveal that during prophase loops are extruded in vivo at ~1-3 kb/sec by condensins as they form a disordered discontinuous helical scaffold within individual chromatids.
2025-12-15 | PXD051785 | Pride
Project description:Untangling of DNA is crucial for the individualization of sister chromatids to prevent errors in chromosome segregation in mitosis. Topoisomerase IIα (TOP2A) plays a pivotal role in this process, serving as the primary enzyme responsible for decatenating sister chromatids. The loop-extrusion activity of condensins at the onset of mitosis produces tension on catenanes, directing TOP2A activity towards decatenation. Consequently, condensins and topoisomerase collaborate in the individualization of sister chromatids. Through a haplo-genetic screen in human cells, we identified a highly conserved protein, S1 RNA-binding domain-containing protein (SRBD1), to be absolutely essential for sister chromatid segregation in WT cells but not in Condensin II-deficient cells. The anaphase defects observed upon loss of SRBD1 strikingly resemble the mitotic defects observed when decatenation is perturbed by inhibition or depletion of TOP2A. Moreover, SRBD1 localizes at the central axis of mitotic chromatids, akin to condensins and TOP2A. We show that the activity of SRBD1 is most critical during prophase, corresponding to the peak of Condensin II and TOP2A activity. We found that SRBD1 exhibits direct DNA binding activity with a preference for single-stranded DNA, implying its action at specific genomic structures. Indeed, we found that SRBD1 is strongly enriched at genomic loci associated to transcription and DNA repair. Altogether, we propose that SRBD1 acts at such locations to promote directionality of TOP2A and to prevent the formation of difficult-to-resolve DNA structures, thereby averting severe chromosome missegregations, a function that seems anciently conserved.
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Project description:Mechanisms of X chromosome dosage compensation have been studied in model organisms with distinct sex chromosome ancestry. However, the diversity of mechanisms as a function of sex chromosome evolution is largely unknown. Here, we anchor ourselves to the nematode Caenorhabditis elegans, where dosage compensation is accomplished by an X chromosome specific condensin that belongs to the family of structural maintenance of chromosomes (SMC) complexes. By combining a phylogenetic analyses of the C. elegans dosage compensation complex with a comparative analysis of its epigenetic signatures, such as X-specific topologically associating domains (TADs) and enrichment of H4K20me1, we show that the condensin-mediated mechanism evolved recently in the lineage leading to Caenorhabditis following an SMC-4 duplication. Unexpectedly, we found an independent duplication of SMC-4 in Pristionchus pacificus along with X-specific TADs and H4K20me1 enrichment, which suggests that condensin-mediated dosage compensation evolved more than once in nematodes. Differential expression analysis between sexes in several nematode species indicates that dosage compensation itself precedes the evolution of X-specific condensins. In Rhabditina, X-specific condensins may have evolved in the presence of an existing mechanism linked to H4K20 methylation as Oscheius tipulae X chromosomes are enriched for H4K20me1 without SMC-4 duplication or TADs. In contrast, Steinernema hermaphroditum lacks H4K20me1 enrichment, SMC-4 duplication, and TADs. Together, our results indicate that dosage compensation mechanisms continue to evolve in species with shared X chromosome ancestry, and SMC complexes may have been co-opted at least twice in nematodes, suggesting that the process of evolving chromosome wide gene regulatory mechanisms are constrained.
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