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HiCAR analysis of zebrafish fin regeneration identifies cis-regulatory chromatin reorganization in response to injury

ABSTRACT: HiCAR analysis of zebrafish fin regeneration identifies cis-regulatory chromatin reorganization in response to injury

PROVIDER: PRJNA967663 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24450700_1.fastq.gz	Fastqsanger.gz
	SRR24450700_2.fastq.gz	Fastqsanger.gz
	SRR24450701_1.fastq.gz	Fastqsanger.gz
	SRR24450701_2.fastq.gz	Fastqsanger.gz
	SRR24450702_1.fastq.gz	Fastqsanger.gz

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HiCAR analysis of zebrafish fin regeneration identifies cis-regulatory chromatin reorganization in response to injury

Project description:HiCAR (Hi-C on accessible regulatory DNA), which is a genome-wide profiling of chromatin accessibility and open chromatin anchored cis-regulatory element (cRE) interactions, identified 28690 calling loops from zebrafish caudal fins at three different time points (0, 1 and 4 day(s) post amputation (dpa)) including 5022 regeneration-responsive loops (17.5%).

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Project description:Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state. Total RNA was extracted from caudal fin at 0, 12, 24 and 48 hours post amputation from STZ treated (DM) and untreated controls.

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