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Elongation factor ELOF1 drives transcription-coupled repairand prevents genome instability [DRB-TTchem-seq]

ABSTRACT: Elongation factor ELOF1 drives transcription-coupled repairand prevents genome instability [DRB-TTchem-seq]

PROVIDER: PRJNA625961 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11563129.fastq.gz	Fastqsanger.gz
	SRR11563130.fastq.gz	Fastqsanger.gz
	SRR11563131.fastq.gz	Fastqsanger.gz
	SRR11563132.fastq.gz	Fastqsanger.gz
	SRR11563133.fastq.gz	Fastqsanger.gz

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Elongation factor ELOF1 drives transcription-coupled repairand prevents genome instability [DRB-TTchem-seq]

Project description:Correct transcription is crucial for life. However, DNA damage severely impedes elongating RNA Polymerase II (Pol II), causing transcription inhibition and transcription-replication conflicts. Cells have evolved intricate mechanisms to counteract the severe consequence of these transcription-blocking lesions, however the exact mechanism and factors involved remain largely unknown. Here, using a genome-wide CRISPR/cas9 screen, we identified elongation factor ELOF1 as an important new factor in the damage-induced transcription stress response. ELOF1 has an evolutionary-conserved role in TC-NER where it promotes the recruitment of the TC-NER factors UVSSA and TFIIH and facilitates Pol II ubiquitylation to efficiently repair TBLs. Importantly, ELOF1 has an additional role in protecting cells from transcription-mediated replication hindrance, thereby preserving genome stability. Thus, ELOF1 protects the transcription machinery from DNA damage by two distinct mechanisms.

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Elongation factor ELOF1 drives transcription-coupled repair and prevents genome instability

Project description:Correct transcription is crucial for life. However, DNA damage severely impedes elongating RNA Polymerase II (Pol II), causing transcription inhibition and transcription-replication conflicts. Cells are equipped with intricate mechanisms to counteract the severe consequence of these transcription-blocking lesions (TBLs). However, the exact mechanism and factors involved remain largely unknown. Here, using a genome-wide CRISPR/cas9 screen, we identified elongation factor ELOF1 as an important new factor in the transcription stress response upon DNA damage. We show that ELOF1 has an evolutionary conserved role in Transcription-Coupled Nucleotide Excision Repair (TC-NER), where it promotes recruitment of the TC-NER factors UVSSA and TFIIH to efficiently repair TBLs and resume transcription. Additionally, ELOF1 modulates transcription to protect cells from transcription-mediated replication stress, thereby preserving genome stability. Thus, ELOF1 protects the transcription machinery from DNA damage via two distinct mechanisms.

2021-04-20 | PXD025304 | Pride

Elongation factor ELOF1 drives transcription-coupled repair and prevents genome instability.

Project description:Correct transcription is crucial for life. However, DNA damage severely impedes elongating RNA polymerase II, causing transcription inhibition and transcription-replication conflicts. Cells are equipped with intricate mechanisms to counteract the severe consequence of these transcription-blocking lesions. However, the exact mechanism and factors involved remain largely unknown. Here, using a genome-wide CRISPR-Cas9 screen, we identified the elongation factor ELOF1 as an important factor in the transcription stress response following DNA damage. We show that ELOF1 has an evolutionarily conserved role in transcription-coupled nucleotide excision repair (TC-NER), where it promotes recruitment of the TC-NER factors UVSSA and TFIIH to efficiently repair transcription-blocking lesions and resume transcription. Additionally, ELOF1 modulates transcription to protect cells against transcription-mediated replication stress, thereby preserving genome stability. Thus, ELOF1 protects the transcription machinery from DNA damage via two distinct mechanisms.

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Effect of transcription inhibitor DRB on gene expression under KRASG12V induction of SAEC

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Small RNA deep sequencing of Arabidopsis DRB mutants

Project description:Arabidopsis thaliana (Arabidopsis) encodes five DOUBLE-STRANDED RNA BINDING (DRB) proteins, DRB1 to DRB5, that predominantly act as non-catalytic cofactors for DICER-LIKE (DCL) proteins in the double-stranded RNA (dsRNA) processing stages of small RNA (sRNA) production pathways. In the nucleus, DRB1 is required for microRNA (miRNAs) processing from imperfectly dsRNA precursors by DCL1. Similarly, DRB4 is required by DCL4 for small-interfering RNAs (siRNAs) production from endogenous or exogenous perfectly dsRNA templates. DRB2 has been recently demonstrated to be required for miRNA and siRNA production in developmentally-important tissues of Arabidopsis while the requirement of either DRB3 or DRB5 in sRNA production remains unclear. Here, we analyse in parallel, the contribution of all five DRB protein family members to the global sRNA landscape of Arabidopsis floral tissues. In depth bioinformatic analysis of sRNA sequencing datasets generated from floral tissues of DRB knockout mutant (drb) plant lines, drb1, drb2, drb4, drb12, drb14, drb24, and drb35 and their comparison to the floral sRNA profile of wild-type Arabidopsis, has enabled confident assignment of the requirement of DRB1, DRB2 and DRB4 for the production of specific miRNA and siRNA subclasses in this tissue. Our analyses have additionally identified novel and/or expanded roles for DRB2 in miRNA, trans-acting siRNAs (tasiRNAs) and natural antisense transcript siRNAs (natsiRNAs) production.

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