摘要
Apoptotic chromatin condensation inducer in the nucleus (also referred as Acin1) was first characterized as an RNA-binding protein involved in apoptosis. In later reports, Acin1 was identified as an auxiliary component of the exon junction complex (EJC) which is assembled throughout pre-messenger RNA splicing. In this study, results of whole-transcriptome analyses revealed reduced expressions and reprogrammed splicing profiles of Acin1 transcripts throughout development of brown adipose tissues (BATs) that execute non-shivering thermogenesis in small rodents and infants by consuming lipids. Depletion of endogenous Acin1 isoforms led to activation of brown adipogenic signatures in mouse C3H10T1/2 fibroblasts. Nevertheless, overexpressions of the Acin1-L or Acin1-S isoform exerted discriminative influences on brown adipogenesis and reprogramming of the expression of serine/arginine-rich splicing factor 3 (SRSF3) through an alternative splicing-coupled nonsense-mediated decay mechanism in a sequence-specific manner. Moreover, the Acin1-SRSF3 axis constitutes a regulatory pathway that participates in the brown adipocyte-related splicing network. Taken together, the interplay between accessory EJC components and splicing regulators constitutes an emerging mechanism for differentially manipulating the activity of brown adipogenesis via alternative splicing network.
原文 | 英語 |
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文章編號 | 194601 |
頁(從 - 到) | 194601 |
期刊 | Biochimica et Biophysica Acta - Gene Regulatory Mechanisms |
卷 | 1863 |
發行號 | 9 |
DOIs | |
出版狀態 | 已發佈 - 9月 1 2020 |
ASJC Scopus subject areas
- 生物物理學
- 結構生物學
- 生物化學
- 分子生物學
- 遺傳學