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The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [ChIP-seq]

ABSTRACT: The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [ChIP-seq]

PROVIDER: PRJNA1106009 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28837680_1.fastq.gz	Fastqsanger.gz
	SRR28837680_2.fastq.gz	Fastqsanger.gz
	SRR28837681_1.fastq.gz	Fastqsanger.gz
	SRR28837681_2.fastq.gz	Fastqsanger.gz
	SRR28837682_1.fastq.gz	Fastqsanger.gz

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The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [S1_Exo7T_ExoT]

Project description:Nucleolytic resection of DNA ends is critical for homologous recombination, but its mechanism is not fully understood, particularly in mammalian meiosis. Here we examine roles of the conserved MRN complex (MRE11, RAD50, and NBS1) through genome-wide analysis of meiotic resection in mice with various MRN mutations, including several that cause chromosomal instability in humans. Meiotic DSBs form at elevated levels but remain unresected if Mre11 is conditionally deleted, thus MRN is required for both resection initiation and regulation of DSB numbers. Resection lengths are reduced to varying degrees in MRN hypomorphs or if MRE11 nuclease activity is attenuated in a conditional nuclease-dead Mre11 model. These findings unexpectedly establish that MRN is needed for longer-range extension of resection, not just resection initiation. Finally, resection defects are additively worsened by combining MRN and Exo1 mutations, and mice that are unable to initiate resection or have greatly curtailed resection lengths experience catastrophic spermatogenic failure. Our results elucidate multiple functions of MRN in meiotic recombination, uncover unanticipated relationships between short- and long-range resection, and establish the importance of resection for mammalian meiosis.

2024-05-06 | GSE266258 | GEO

The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [SSDS]

2024-05-06 | GSE266271 | GEO

The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [ChIP-seq]

2024-05-06 | GSE266151 | GEO

The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [S1_Exo7T_ExoT]

Project description:The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [S1_Exo7T_ExoT]

| PRJNA1106461 | ENA

The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [SSDS]

Project description:The MRE11-RAD50-NBS1 complex both starts and extends DNA end resection in mouse meiosis [SSDS]

| PRJNA1106485 | ENA

MRE11-RAD50-NBS1 activates Fanconi Anemia R-loop suppression at transcription-replication conflicts

Project description:Rad50 is a component of the conserved MRE11-RAD50-NBS1 (MRN) complex, which functions in genome stability and the cell’s ability to deal with stalled DNA replication forks. We identified Rad50 as a factor important for R-loop tolerance and thus mapped DNA:RNA hybrids in Rad50KO cells and compare them to previously reported wild-type and Sgs1KO profiles.

2019-10-31 | E-MTAB-7885 | biostudies-arrayexpress

PPARG interactions with UBR5 and MRE11-RAD50-NBS1 are required for DNA damage response and repair.

Project description:PPARG interactome datasets containing (1) Flag-PPARG AP-MS, identifying MRE11, RAD50 and NBS1 as novel interactors, (2) tandem-IP (in solution and silver fragments) of PPARG-Strep and Flag-NBS1, which identifies PPARG interaction with UBR5 (3) tandem-IP (same as 2) with BS3 cross-linking illustrates the binding interface between PPARG and NBS1. These mass spec data and other biochemical data demonstrate PPARG novel roles in promoting DNA damage response and repair, by activating the ATM pathway.

2018-12-18 | MSV000083257 | MassIVE

Gene Expression Profile of Deletion RAD50, MRE11, XRS2

Project description:Deletion mutants of the yeast MRX complex (Rad50, Mre11 and Xrs2) were studied for gene expression levels. Significant difference in expression levels was observed in genes pertaining to DNA damage, cell cycle etc. as compared to the BY4741 wild type.

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A Rad50-null mutation in mouse germ cells causes reduced DSB formation, abnormal DSB end resection and complete loss of germ cells

Project description:Programed DNA double-strand breaks (DSBs) catalyzed by the topoisomerase II-like enzymes, SPO11 and TOPVIBL, initiate meiotic recombination. Following DSB formation, the MRE11-RAD50-NBS1/Xrs2 (MRN/X) complex, along with EXO1 and DNA2, cleave the SPO11-DNA to generate 3′ single-stranded DNA (ssDNA) ends, which are prerequisite for meiotic DSB repair. In both yeast and mammals, MRE11 exhibits endonucleolytic cleavage of the 5′ terminated DNA strand in the vicinity of the DSBs and exonucleolytic resection from 3′ to 5′ towards the DSB ends. RAD50 is a structure maintenance of chromosome (SMC) related protein that contains one ATPase domain at its N- and C- terminal ends, respectively, Zn hook, and anti-parallel coiled coils. RAD50 plays a crucial role in facilitating the MRE11 nuclease activity on DSBs by ATP binding and hydrolysis. However, the in vivo function of Rad50 in mammalian germ cells, particularly its in vivo role in the resection of meiotic DSB ends at the molecular level remains elusive. Here, we performed END-seq with synchronized zygotene spermatocytes from control and germ cell specific Rad50 mutant (Rad50-sKO) mice. We find that the number of formed DSB in the mutant spermatocytes was reduced compared to control spermatocytes (6 636 DSBs in Rad50-sKO spermatocytes vs 8 168 in control spermatocytes) and abnormal DSB end resection occurred in mutant spermatocytes (DSB end resection length: 1 279 nts in Rad50-sKO spermatocytes vs 1 923 nts in control spermatocytes). Thus, RAD50 is essential for DSB formation and end resection during mammalian meiosis.

2024-04-02 | GSE262706 | GEO

Genome-wide expression analysis in murine liver after Nbs1 induced knockout

Project description:NBS1 (Nbn in Mus musculus) is a critical component of the MRN (MRE11/RAD50/NBS1) complex, which regulates ATM- and ATR-mediated DNA damage response (DDR) pathways. NBS1 mutations cause the human genomic instability syndrome Nijmegen Breakage Syndrome (NBS), in which microcephaly and intellectual disability are marked neuronal deficits. NBS1 is essential for life, because of its function in the DDR to ensure proliferation and preventing the cell death of replicating cells. However, the function of NBS1 in postmitotic cells is unclear. To explore the possible role of Nbs1 in non-dividing cells and the effection of its deletion on gene expression, RNA-seq was carried out with Nbs1 induced knockout liver samples, in which most cells are postmitotic.

2022-09-16 | GSE137505 | GEO

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