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Identification of Alternative Splicing and Polyadenylation in RNA-seq Data
Published on: June 24, 2021
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Alternative polyadenylation dependent function of splicing factor SRSF3 contributes to cellular senescence
Ting Shen1, Huan Li1, Yifang Song1
1State Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center of Genetics and Development, Human Phenome Institute, School of Life Sciences and Huashan Hospital, Fudan University, Shanghai 200438, China.
Aging
|March 6, 2019
Summary
Reduced splicing factor SRSF3 promotes cellular senescence via alternative polyadenylation (APA). This mechanism involves 3' untranslated region shortening, impacting protein production and senescence pathways.
Area of Science:
- Molecular Biology
- Cellular Biology
- Genetics
Background:
- Splicing factor SRSF3 downregulation is linked to cellular senescence.
- Cellular senescence plays a role in cancer prevention and aging.
Purpose of the Study:
- To investigate the alternative polyadenylation (APA) dependent function of SRSF3 in cellular senescence.
- To elucidate the novel mechanism by which SRSF3 downregulation induces senescence.
Main Methods:
- Knockdown of SRSF3 in human and mouse cells.
- Analysis of alternative polyadenylation and 3' untranslated region (3' UTR) lengths.
- Gene expression and protein production analysis.
- Overexpression of candidate genes (PTEN, PIAS1, DNMT3A) and AKT phosphorylation assays.
Main Results:
- SRSF3 knockdown led to proximal poly(A) site usage and global 3' UTR shortening.
- 3' UTR shortened genes were enriched in senescence-associated pathways.
- Overexpression of PTEN, PIAS1, and DNMT3A mimicked senescence phenotypes.
- SRSF3 binds near proximal poly(A) sites; PTEN upregulation reduced AKT phosphorylation, inducing senescence.
Conclusions:
- Reduced SRSF3 expression promotes cellular senescence through an APA-dependent mechanism.
- This study reveals a novel pathway linking splicing factors to senescence.
- Findings advance the understanding of splicing factor-regulated cellular senescence.
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