RAD51 family members remodel the NHEJ system to modulate stress-induced biosynthesis of diterpenoid phytoalexins in rice
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ABSTRACT:
PROVIDER: PRJNA1214213 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32086346_1.fastq.gz | Fastqsanger.gz | |||
| SRR32086346_2.fastq.gz | Fastqsanger.gz | |||
| SRR32086347_1.fastq.gz | Fastqsanger.gz | |||
| SRR32086347_2.fastq.gz | Fastqsanger.gz | |||
| SRR32086348_1.fastq.gz | Fastqsanger.gz |
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Project description:Double-strand break (DSB) damage are primarily repaired via homologous recombination (HR) and non-homologous end joining (NHEJ) in Eukaryotes. We reveals that HR subcomplex RAD51A1-RAD51C in rice (Oryza sativa L.) inhibits classic NHEJ pathway while acts as a transcriptional mediator underlying alternative NHEJ signaling. RAD51C hijacks the KU70 at DSBs, facilitated by the interacting partner RAD51A1 or TOP6B responding environmental cues (pathogens and 4℃). Consequently, the enhanced alternative NHEJ signaling generates the phosphorylated SOG1, which activates the regulatory network in diterpenoid phytoalexin biosynthesis and a group of genes in phenylpropanoid pathway. Intriguingly, SOG1-BRCA1-RAD51 associates with RAD51C-RAD51D-XRCC3 forming a transcription pre-initiation complex in this process. Phenotypically, chemical disease resistance and 4℃-conditioned stomatal closure are compromised in single mutants (atm-3, sog1, and rad51c-1), double mutants (rad51a1 rad51a2 and rad51d xrcc3). In summary, HR pathway integrates classic and alternative NHEJ pathways to orchestrate stress-activated specific metabolism in rice plants. Hierarchical functional collaboration of global DSB-repair machinerys enable plant adaptability to DSB-related environmental stresses.
2025-01-27 | GSE287659 | GEO
Project description:Double-strand break (DSB) damage are primarily repaired via homologous recombination (HR) and non-homologous end joining (NHEJ) in Eukaryotes. We reveals that HR subcomplex RAD51A1-RAD51C in rice (Oryza sativa L.) inhibits classic NHEJ pathway while acts as a transcriptional mediator underlying alternative NHEJ signaling. RAD51C hijacks the KU70 at DSBs, facilitated by its partner RAD51A1 or TOP6B responding environmental cues (pathogens and 4℃). Consequently, the enhanced alternative NHEJ signaling generates the phosphorylated SOG1, which activates the regulatory network in diterpenoid phytoalexin biosynthesis and a group of enzyme genes in phenylpropanoid pathway. Intriguingly, SOG1-BRCA1-RAD51 associates with RAD51C-RAD51D-XRCC3 to form a transcription pre-initiation complex in this process. Phenotypically, chemical disease resistance and 4℃-conditioned stomatal closure are compromised in single mutants (atm-3, sog1, and rad51c-1), double mutants (rad51a1 rad51a2 and rad51d xrcc3). In summary, HR pathway integrates classic and alternative NHEJ pathways to orchestrate stress-activated specific metabolism in rice. Hierarchical collaboration of global DSB-repair machinerys enable plant adaptability to DSB-related environmental stresses.
2025-01-30 | GSE288025 | GEO
Project description:RAD51 family factors remodel the NHEJ system to modulate stress-induced biosynthesis of diterpenoid phytoalexins in rice.
| PRJNA1215736 | ENA
Project description:Cells have developed effective mechanisms, namely homologous recombination (HR) and non-homologous end-joining (NHEJ), to repair DNA double-strand breaks (DSBs), which are considered to be the most deleterious type of damage that can challenge genome integrity. While these pathways coexist to repair DSBs, the mechanisms by which one of these pathways is chosen to repair a particular DSB remain unclear. Here, we show that the chromatin context in which a break occurs participates in this choice and that transcriptionnaly active chromatin channels repair to HR. By using a human cell line expressing a restriction enzyme fused to the ligand binding domain of the oestrogen receptor (AsiSI-ER)2,3, together with a genome wide chromatin immunoprecipitation-sequencing (ChIP-seq) approach, we establish that distinct DSBs induced across the genome are not necessarily repaired by the same pathway. Indeed, we identify an HR-prone subset of DSBs that recruit the HR protein RAD51, undergo resection, and rely on RAD51 for efficient repair. These DSBs are located in actively transcribed genes, and repair at such DSBs can be switched to RAD51-independent repair pathway upon transcriptional inhibition. Moreover, we show that HR is targeted to transcribed loci thanks to the elongation-associated H3K36me3 histone mark. Indeed depletion of HYPB, the main H3K36 tri methyltransferase severally impedes the use of HR at those DSBs. Our study, thereby demonstrates a clear role for chromatin in DSB repair pathway choice in human cells.
2014-03-23 | E-MTAB-1241 | biostudies-arrayexpress
Project description:RAD51 is a highly conserved DNA repair protein and is indispensable for the execution of homologous recombination, thereby participating in maintaining genomic stability. Since constitutive Rad51 knockout mice exhibit embryonic lethality, the physiological functions of RAD51, and the consequences of lacking it, are largely unknown. We herein demonstrated a critical role of RAD51 in postnatal liver development and regeneration. RAD51 is highly expressed during liver development and during regeneration following hepatectomy and hepatic injury, and is also elevated in liver-related diseases. We generated hepatocyte-specific Rad51 deletion mouse model (Rad51-CKO) to evaluate the function of RAD51 in liver development and regeneration.RAD51 deletion in postnatal hepatocytes results in aborted mitosis, global polyploidization, oxidative stress and cellular senescence. Remarkable liver fibrosis occurs as early as in 3-month-old Rad51fl/fl; Alb-Cre+/+ mice.The senescence-associated secretory phenotype in the livers of Rad51-CKO mice creates a niche that favors the activation and propagation of hepatic progenitor cells (HPCs) in which Rad51 is spared due to lack of Alb-Cre expression. The Rad51 functional HPCs and immature hepatocytes can thus proliferate vigorously, acquire increased malignancy, and eventually give rise to HCC. Our results thus demonstrate a novel function of RAD51 in liver development, homeostasis and tumorigenesis. The RAD51-CKO mice represent a unique genetic model for premature liver senescence, fibrosis, impaired regeneration and hepatocellular carcinogenesis.
2025-01-22 | GSE243719 | GEO
Project description:RAD51 is a highly conserved DNA repair protein and is indispensable for the execution of homologous recombination, thereby participating in maintaining genomic stability. Since constitutive Rad51 knockout mice exhibit embryonic lethality, the physiological functions of RAD51, and the consequences of lacking it, are largely unknown. We herein demonstrated a critical role of RAD51 in postnatal liver development and regeneration. RAD51 is highly expressed during liver development and during regeneration following hepatectomy and hepatic injury, and is also elevated in liver-related diseases. We generated hepatocyte-specific Rad51 deletion mouse model (Rad51-CKO) to evaluate the function of RAD51 in liver development and regeneration.RAD51 deletion in postnatal hepatocytes results in aborted mitosis, global polyploidization, oxidative stress and cellular senescence. Remarkable liver fibrosis occurs as early as in 3-month-old Rad51fl/fl; Alb-Cre+/+ mice.The senescence-associated secretory phenotype in the livers of Rad51-CKO mice creates a niche that favors the activation and propagation of hepatic progenitor cells (HPCs) in which Rad51 is spared due to lack of Alb-Cre expression. The Rad51 functional HPCs and immature hepatocytes can thus proliferate vigorously, acquire increased malignancy, and eventually give rise to HCC. Our results thus demonstrate a novel function of RAD51 in liver development, homeostasis and tumorigenesis. The RAD51-CKO mice represent a unique genetic model for premature liver senescence, fibrosis, impaired regeneration and hepatocellular carcinogenesis.
2025-01-22 | GSE243614 | GEO
Project description:DNA double strand breaks (DSBs) are a major source of mutations. Both non-homologous-end-joining (NHEJ) and microhomology-mediated-end-joining (MMEJ) DSB repair pathways are error prone and produce deletions, which can lead to cancer. DSBs also lead to epigenetic changes, including demethylation, which is involved in carcinogenesis. Of specific interest is the MMEJ repair pathway, as it requires methylation restoration around the break, as a result of the resection and formation of single stranded (ssDNA) intermediates. While, methylation patterns after homologous recombination (HR) have been partially studied, the methylation status after MMEJ and NHEJ remains poorly reported, and can be relevant for cancer. To study methylation patterns around DSB after NHEJ and MMEJ repair, we used targeted bisulfite-sequencing (BS-seq) to quantify methylation of dozens of single cell clones after induction of DSB by CRISPR. Each single cell clone was classified according to the sequence signature to a specific repair mechanism: NHEJ or MMEJ. Comparison of single cell clones after DSB to control cells, without DSB, demonstrated correct restoration of the methylation levels. No difference in methylation patterns was noticed when comparing NHEJ to MMEJ. Methylation levels in gene body, highly methylated CpGs (n=61, 4000 base pairs around DSB) and in low methylation CpGs (n=19), remained stable after both MMEJ and NHEJ. Gene body methylation persisted even on the background of DNMT3A R882C mutation, the most prevalent preleukemic mutation, in which the de novo methylation machinery is compromised. An exception observed in a single CpG site (ASXL1 995) which demonstrated elevated methylation rate after DSB repair only in the presence of WT DNMT3A. In summary, DNA methylation restoration demonstrated high fidelity after DSB both in methylated and unmethylated gene body, even in cases where DNA resections and deletions occurred.
2022-09-11 | E-MTAB-12037 | biostudies-arrayexpress
Project description:Purpose: The recombinant endonucleases introduce double-strand breaks (DSBs) in genomic DNA at targeted sites and non-homologous end-joining (NHEJ) pathways repair the breaks introducing indels into the genome. To investigate whether there is another NHEJ pathway or if A-NHEJ and C-NHEJ are redundant, we examined NHEJ edits in HeLa cells. Methods: To test among these possibilities, we engineered a NHEJ reporter system using targeted TALEN induced double strand DNA breaks. C-NHEJ was blocked in XRCC4(-/-) cells and A-NHEJ was blocked pharmacologically with mirin. To assess how NHEJ was maintained, differentially expressed genes were determined by RNA-Seq. Results: When both C-NHEJ and A-NHEJ are blocked, edits were still observed. No changes in expression of DNA repair genes was observed. However, when both NHEJ pathways were blocked, genes from several pathways including DNA damage response, hypoxic response, chromatin packaging, p53 response and two genes that stimulate homologous recombination were differentially expressed. Conclusions: NHEJ is maintained when both NHEJ pathways are blocked through a transcriptional response that must compensate for the inhibited steps in both pathways.
2020-12-31 | GSE135274 | GEO
Project description:Long non-coding RNAs (lncRNA) have been shown to play crucial roles in tumorigenesis. Little is known about lncRNA RAD51-AS1 in diseases. Here, we investigated the role of RAD51-AS1 in Epithelial ovarian cancer. Silencing RAD51-AS1 inhibited proliferation through cell cycle arrest and promotion in apoptosis, both in vitro and in vivo. But the mechanism of RAD51-AS1 downstream regulation remains unclear. In order to identify the downstream regulation of RAD51-AS1 in epithelial ovarian cancer, we used antisene oligotides targeting RAD51-AS1 / negative control to transfect Skov3.ip cells. Then, we used microarrays to identified differential expression genes and to look for possible target genes by knockdown RAD51-AS1 expression.
2017-08-17 | GSE89374 | GEO
Project description:RAD51, a multifunctional protein, plays a central role in DNA replication and homologous recombination repair, and is known to be involved in cancer development. We identified a novel role for RAD51 in innate immune response signaling. Defects in RAD51 lead to the accumulation of self-DNA in the cytoplasm, triggering a STING-mediated innate immune response after replication stress and DNA damage. Our data suggest that in addition to playing roles in homologous recombination-mediated DNA double-strand break repair and replication fork processing, RAD51 is also implicated in the suppression of innate immunity. Thus, our study reveals a previously uncharacterized role of RAD51 in initiating immune signaling, placing it at the hub of new interconnections between DNA replication, DNA repair, and immunity.
2017-02-18 | GSE95050 | GEO