Ontology highlight
ABSTRACT:
PROVIDER: PRJNA675404 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13012700_1.fastq.gz | Fastqsanger.gz | |||
| SRR13012700_2.fastq.gz | Fastqsanger.gz | |||
| SRR13012701_1.fastq.gz | Fastqsanger.gz | |||
| SRR13012701_2.fastq.gz | Fastqsanger.gz | |||
| SRR13012702_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study we used mice lacking Evf2 (Evf2TS/TS) and mice expressing a truncated form of Evf2 (Evf1TS/TS) to determine UCE lncRNA epigenetic and chromosome toplogical control. We used 4Cseq to investigate how Evf2 regulates UCE interactions along chromosome 6 (where Evf2 is expressed). We used ChIpseq to compare histone methylation profiles from Evf2TS/TS and Evf1TS/TS. In addition, we used ChIPseq to determine Evf2-depedent regulation of cohesin subunit binding (SMC1 and SMC3) and histone H3K27acetylation. Together, these data support that Evf2 UCE lncRNA controls chromosome topology over multi-megabse distances, through cohesin binding and effects on histone methylation and acetylation. Also included is the ChIPseq profile of Dlx binding sites in SW (outbred strain of mice) from E13.5 GE.
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Project description:ARP/ASCL transcription factors are key determinants of cell fate specification in a wide variety of tissues, coordinating the acquisition of generic cell fates and of specific subtype identities. How these factors, recognizing highly similar DNA motifs, display specific activities, is not yet fully understood. To address this issue, we overexpressed different ARP/ASCL factors in zebrafish ascl1a-/- mutant embryos to determine which one is able to rescue the intestinal secretory lineage. We found that Ascl1a/b, Atoh1a/b and Neurod1 factors are all able to trigger the first step of the secretory regulatory cascade but distinct secretory cells are induced by these factors. Indeed, Neurod1 rescues the enteroendocrine lineage while Ascl1a/b and Atoh1a/b rescue the goblet cells. Gain-of-function experiments with Ascl1a/Neurod1 chimeric proteins revealed that the functional divergence is encoded by a 19-aa ultra-conserved element (UCE), present in all Neurod members but absent in the other ARP/ASCL proteins. This novel domain acts as a goblet cell fate repressor and inhibits Gfi1aa expression, known to be important for goblet cell differentiation. Deleting the UCE domain of the endogenous Neurod1 protein leads to an increase in the number of goblet cells concomitant with a reduction of several EE subtypes, validating the importance of the UCE domain in enteroendocrine cell differentiation. Importantly, the neurod1 null mutant displays very similar defects supporting the crucial function of the UCE domain for NeuroD1 activity in the intestine. As Gfi1 acts as a binary cell fate switch in several tissues where Neurod1 is also expressed, we can envision a similar role of the UCE in other tissues, allowing Neurod1 to repress Gfi1 to influence the balance between cell fates.
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