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Balanced SET levels favor the correct enhancer repertoire during cell fate acquisition

ABSTRACT: Balanced SET levels favor the correct enhancer repertoire during cell fate acquisition

PROVIDER: PRJNA874714 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21307319_1.fastq.gz	Fastqsanger.gz
	SRR21307319_2.fastq.gz	Fastqsanger.gz
	SRR21307320_1.fastq.gz	Fastqsanger.gz
	SRR21307320_2.fastq.gz	Fastqsanger.gz
	SRR21307321_1.fastq.gz	Fastqsanger.gz

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Balanced SET levels favor the correct enhancer repertoire during cell fate acquisition.

Project description:Within the chromatin, distal elements interact with promoters to regulate specific transcriptional programs. Histone acetylation, interfering with the net charges of the nucleosomes, is a key player in this regulation. Here, we report that the oncoprotein SET is a critical determinant for the levels of histone acetylation within enhancers. We disclose that a condition in which SET is accumulated, the severe Schinzel-Giedion Syndrome (SGS), is characterized by a failure in the usage of the distal regulatory regions typically employed during fate commitment. This is accompanied by the usage of alternative enhancers leading to a massive rewiring of the distal control of the gene transcription. This represents a (mal)adaptive mechanism that, on one side, allows to achieve a certain degree of differentiation, while on the other affects the fine and corrected maturation of the cells. Thus, we propose the differential in cis-regulation as a contributing factor to the pathological basis of SGS and possibly other the SET-related disorders in humans.

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Balanced SET levels favor the correct enhancer repertoire during cell fate acquisition

Project description:To understand the effect of SET protein accumulation on genomic function we used different accumulating models, cells and in vivo, that we analyzed with different techinques up to the single level. SET accumulation is known to be caused by the accumulation of its direct interactor SETBP1, when mutated, the causative gene of Schinzel Giedion syndrome. SET has been shown to be able to interfere with histones acetylation, thus we wanted to investigated the functional effect on the genome function and cell fate commitment.

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