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Mus musculus

ABSTRACT: Genome-wide analysis of tumor suppressive programs during p53-induced regression of Myc-driven lymphomas [RNA-Seq]

PROVIDER: PRJNA318258 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3363030_1.fastq.gz	Fastqsanger.gz
	SRR3363030_2.fastq.gz	Fastqsanger.gz
	SRR3363040_1.fastq.gz	Fastqsanger.gz
	SRR3363040_2.fastq.gz	Fastqsanger.gz
	SRR3363050_1.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of tumor suppressive programs during p53-induced regression of Myc-driven lymphomas

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Project description:For the most frequently inactivated tumor suppressor p53, genetic mouse models have demonstrated regression of p53-null tumors upon p53 reactivation. While this was shown in tumor models driven by p53 loss as the initiating lesion, many tumors initially develop in the presence of wild-type p53, acquire aberrations in the p53 pathway to bypass p53-mediated tumor suppression, and inactivate p53 itself only at later stages during metastatic progression or therapy. To explore the efficacy of p53 reactivation in this scenario, we used a reversibly switchable p53 (p53ERTAM) mouse allele to generate Eµ-Myc-driven lymphomas in the presence of active p53 and, after full lymphoma establishment, switched off p53 to model late-stage p53 inactivation.

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Genome-wide analysis of tumor suppressive programs during p53-induced regression of Myc-driven lymphomas [ChIP-Seq]

Project description:The tumor suppressor p53 is a transcription factor that controls the response to stress. Here, we dissected the transcriptional programs triggered upon restoration of p53 in Myc-driven lymphomas, based on the integrated analysis of p53 genomic occupancy and gene regulation. p53 binding sites were identified at promoters and enhancers, both characterized by the pre-existence of active chromatin marks. p53 recruitment at these sites was mainly mediated through protein-protein or protein-chromatin interactions and, only for a small fraction, through recognition of the 20 base-pair p53 consensus motif. At promoters, p53 binding to the consensus motif was associated with gene induction, but not repression, indicating that the latter was most likely indirect. p53 also targeted unmarked distal sites devoid of activation marks, at which binding was prevalently driven by recognition of the consensus motif. At all sites, our data highlighted a functional role for the canonical, unsplit consensus element, but did not provide evidence for p53 recruitment by split motifs. Altogether, our data highlight key features of genome recognition by p53 and provide unprecedented insight into the pathways associated with p53 re-activation and tumor regression.

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