SUMOylation Regulates miR-34b/c Targeted Gene Expression Program
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA393841 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5817530.fastq.gz | Fastqsanger.gz | |||
| SRR5817531.fastq.gz | Fastqsanger.gz | |||
| SRR5817623.fastq.gz | Fastqsanger.gz | |||
| SRR5817624.fastq.gz | Fastqsanger.gz | |||
| SRR5817625.fastq.gz | Fastqsanger.gz |
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Project description:SUMOylation Regulates miR-34b/c Targeted Gene Expression Program [RNA-seq]
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:The miR-34 family of microRNAs consisting of miR-34a, miR-34b and miR-34c are tumour suppressors. The annotated human miR-34b-5p has one additional base at the 5’ end of the common miR-34 family seed sequence, compared to miR-34a-5p and miR-34c-5p. This extra base results in a shift of the seed sequence, which would affect the target gene repertoire and have functional consequences. During our studies of miR-34 functions, we investigated the precise sequence of mature miR-34b-5p in human cells by deep sequencing. We found that a miR-34b-5p without the extra base was the predominant form in both non-malignant and malignant cells derived from several human tissues, indicating that the miR-34b annotation is misleading. We evaluated the functional implications of the seed shift, by comparing the effect of mimics representing the alternative miR-34b-5p sequences in MDA-MB-231 cells. In contrast to the annotated miR-34b, the endogenously expressed miR-34b displayed tumour suppressive characteristics in vitro similarly to miR-34c. These data demonstrate the importance of determining the precise sequence of a mature microRNA before exploring miRNA functions.
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Project description:Genome wide localization of SUMO1 and SUMO2/3 proteins revealed an asscociation of SUMO proetins with active chromatin. SUMO proteins are enriched at super enhancers and enhancers and SUMOylation regulates a subset of these super enhancers. Super enhancers regulated by SUMOylation were enriched for transcription factor TFAP2C and SUMOylation negatively regulates TFAP2C localization to enhancers and super enhancers. Proteomics and ChIP-PCR at MYC SE suggests that chromatin bound TFAP2C recruits histone deacetylation complexes that increases upon SAE2 knockdown. Conversely, SUMOylation promoted TFAP2C asscociation with pre-mRNA splicing machinery components. Taken together, our study revealed a critical role of SUMOylation in chromatin modification through an AP-2 family of transcription factor, TFAP2C and a potential role of TFAP2C in pre-mRNA splicing.
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