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Comparative analysis of the transcriptional response to bulky DNA damages

ABSTRACT: Comparative analysis of the transcriptional response to bulky DNA damages

PROVIDER: PRJNA986894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25010515.fastq.gz	Fastqsanger.gz
	SRR25010516.fastq.gz	Fastqsanger.gz
	SRR25010517.fastq.gz	Fastqsanger.gz
	SRR25010518.fastq.gz	Fastqsanger.gz
	SRR25010519.fastq.gz	Fastqsanger.gz

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Comparative analysis of the transcriptional response to bulky DNA damages

Project description:A systematic RNA-seq study comparing the transcriptional response to three independent bulky DNA damage inducing agents: UV, the chemotherapy cisplatin and benzo[a]pyrene, a component of cigarette smoke. It was performed in 2 different cell lines - GM12878 immortalized lymphoblast cell line and A549 lung cancer cell line.

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Gene architecture is a determinant of the transcriptional response to bulky DNA damages.

Project description:Bulky DNA damages block transcription and compromise genome integrity and function. The cellular response to these damages includes global transcription shutdown. Still, active transcription is necessary for transcription-coupled repair and for induction of damage-response genes. To uncover common features of a general bulky DNA damage response, and to identify response-related transcripts that are expressed despite damage, we performed a systematic RNA-seq study comparing the transcriptional response to three independent damage-inducing agents: UV, the chemotherapy cisplatin, and benzo[a]pyrene, a component of cigarette smoke. Reduction in gene expression after damage was associated with higher damage rates, longer gene length, and low GC content. We identified genes with relatively higher expression after all three damage treatments, including NR4A2, a potential novel damage-response transcription factor. Up-regulated genes exhibit higher exon content that is associated with preferential repair, which could enable rapid damage removal and transcription restoration. The attenuated response to BPDE highlights that not all bulky damages elicit the same response. These findings frame gene architecture as a major determinant of the transcriptional response that is hardwired into the human genome.

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Project description:The environmental carcinogen, (±)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), causes bulky-adduct DNA damages, triggers certain signaling pathways, and elicits gene expression changes. Here, we focused on the temporal gene expression changes induced by a low concentration (0.05 µM) BPDE in human amnion epithelial FL cells. Differential gene expression profiles at 1, 10 and 22 h post BPDE treatment were obtained using Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays. A cohort of gene expression changes related to cell cycle progression, cell growth or apoptosis, stress response, and post-transcriptional regulation was validated with quantitative real-time RT-PCR. The alteration of several cell cycle-related genes was correlated and possibly contributed to the cell cycle arrest phenotype. Paradoxical transcriptional regulations regarding cell growth or apoptosis emerged in response to BPDE treatment, which indicated that cell fate was determined by integrated signals. The temporal transcriptional changes would be of help to clarify the molecular mechanism of cellular response to BPDE. Keywords: time course

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