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Mus musculus

ABSTRACT: Site-specific DICER and DROSHA RNA products control the DNA damage response

PROVIDER: PRJDB1767 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR001952.fastq.gz	Fastqsanger.gz
	DRR001953.fastq.gz	Fastqsanger.gz
	DRR001954.fastq.gz	Fastqsanger.gz

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DROSHA and DICER RNA products control BMI1-dependent transcriptional repression at DNA damage sites

Project description:DROSHA and DICER RNA products control BMI1-dependent transcriptional repression at DNA damage sites

| PRJNA798043 | ENA

DROSHA and DICER RNA products control BMI1-dependent transcriptional repression at DNA damage sites

Project description:Genome integrity is safeguarded by the DNA damage response (DDR). Transcriptional modulation of genes around DNA double-strand breaks (DSBs) is important for DNA repair. It has been shown that DSBs repress transcription of DSB-bearing genes in an ATM- and PRC1-dependent manner. However, DSB also induce local de novo transcription of non-coding RNA, which are processed by DROSHA and DICER into small DNA-damage-response RNA (DDRNA). Here we reconcile these apparently contrasting observations by showing that DROSHA and DICER inactivation prevents transcriptional repression of DSB-bearing genes by reducing PRC1 recruitment to DSB and consequent H2A-K119 chromatin ubiquitination. Indeed, DDRNAs generated at DSB associate with the PRC1 component BMI1 and inhibition of DDRNA function with antisense oligonucleotides is sufficient to reduce damage-induce transcriptional silencing in cis genes (DISC). We propose that DROSHA, DICER and DDRNAs control DISC at genomic lesion sites by favoring PRC1-driven chromatin ubiquitination.

2025-10-09 | GSE193821 | GEO

Mus musculus

Project description:Expression profile of control, Drosha or Dicer deleted LSKs

| PRJNA260712 | ENA

DROSHA is recruited to DNA damage sites by the MRN complex to promote non-homologous end-joining

Project description:The DNA damage response (DDR) is the signaling cascade that recognizes DNA double-strand breaks (DSB) and promotes their resolution via the DNA repair pathways of Non-Homologous End Joining (NHEJ) or Homologous Recombination (HR). We and others have shown that DDR activation requires DROSHA. However, whether DROSHA exerts its functions by associating with damage sites, what controls its recruitment and how DROSHA influences DNA repair, remains poorly understood. Here we show that DROSHA associates to DSBs independently from transcription. Neither H2AX, nor ATM nor DNA-PK kinase activities are required for its recruitment to break site. Rather, DROSHA interacts with RAD50 and inhibition of MRN by Mirin treatment abolishes this interaction. MRN inactivation by RAD50 knockdown or mirin treatment prevents DROSHA recruitment to DSB and, as a consequence, also 53BP1 recruitment. During DNA repair, DROSHA inactivation reduces NHEJ and boosts HR frequency. Indeed, DROSHA knockdown also increase the association of downstream HR factors such as RAD51 to DNA ends. Overall, our results demonstrate that DROSHA is recruited at DSBs by the MRN complex and direct DNA repair toward NHEJ.

2021-03-15 | GSE166631 | GEO

Expression profile of control, Drosha or Dicer deleted LSKs

2015-09-10 | GSE61305 | GEO

Expression profile of control, Drosha or Dicer deleted LSKs

Project description:To determine genes regulated independently of microRNAs in early haematopoietic progenitors (LSKs) we compared the expression profiles of Drosha or Dicer deficient LSKs and control. Those genes differentially expressed between Drosha or Dicer deficient LSKs are likely regulated indepedently of microRNAs as either Drosha or Dicer deletion will lead to a complete and equivalent loss of microRNAs. LSKs were sorted from control, Drosha fl/fl of Dicer fl/fl mice.These cells were activated in vitro for 72 hours to induce total and equivalent deletion of Drosha or Dicer. RNA was extracted after 72 hours.3 repeats of the three groups were analyzed.

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Nuclear phosphorylated Dicer processes double-stranded RNA in response to DNA damage

Project description:The endonuclease Dicer is a key component of the human RNA interference (RNAi) pathway and known for its role in cytoplasmic micro RNA (miRNA) production. Recent findings suggest that non-canonical Dicer generates small non-coding RNA (ncRNA) to mediate the DNA damage response (DDR). Here we show that human Dicer is phosphorylated in the platform-PAZ-connector helix cassette (S1016) upon induction of DNA damage. Phosphorylated Dicer (p-Dicer) accumulates in the nucleus and is recruited to DNA double-strand breaks (DSBs). We further demonstrate that turnover of damage-induced nuclear dsRNA requires additional phosphorylation of carboxy-terminal Dicer residues (S1728 and S1852). DNA damage-induced nuclear Dicer accumulation is conserved in mammals. Dicer depletion causes spontaneous DNA damage and delays DNA repair. Taken together, we place Dicer in context of the DDR by demonstrating DNA damage-inducible phospho-switch that causes localised processing of nuclear dsRNA by p-Dicer to promote DNA repair.

2018-12-08 | GSE75892 | GEO

Small RNA profiling of RNase III enzyme deficient DN3 thymocytes, Tregs, activated CD4+ T cells, and embryonic fibroblasts

Project description:Here we analyze the small RNA species in the following: 1. DN3 thymocytes following inactivation of LoxP flanked Drosha and Dicer alleles with Lck-cre 2. Tregs following inactivation of LoxP flanked Drosha and Dicer alleles with CD4-cre 3. activated CD4+ T cells following inactivation of LoxP flanked Drosha and Dicer alleles with CD4-cre 4. MEFs following inactivation of LoxP flanked Drosha and Dicer alleles with Rosa26-CreER and 4-OH tamoxifen treatment

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small RNA profiling of breast cancer cell lines [knockdowns]

Project description:We performed small RNA sequencing in breast cancer cells treated with siRNA for Control, DCGR8, DROSHA, TARBP2, DICER

2018-11-07 | GSE114773 | GEO

RNA expression in mutants of the miRNA pathway during myelination

Project description:RNA sequencing was performed comparing sciatic nerves of Schwann cell specific DICER mutants with SC-specific DGCR8 and DROSHA mutants.

2018-10-08 | GSE64880 | GEO

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