| Literature DB >> 35588208 |
Mei Guo1, Chunhai Luo2, Zhuqing Wang3,4, Sheng Chen4,5, Dayton Morris4, Fengying Ruan1, Zhichao Chen1, Linfeng Yang1, Xiongyi Wei2, Chuanwen Wu1, Bei Luo1, Zhou Lv1, Jin Huang1, Dong Zhang1, Cong Yu1, Qiang Gao1, Hongqi Wang1, Ying Zhang2, Fei Sun2, Wei Yan3,4,6, Chong Tang1,2.
Abstract
As one of the post-transcriptional regulatory mechanisms, uncoupling of transcription and translation plays an essential role in development and adulthood physiology. However, it remains elusive how thousands of mRNAs get translationally silenced while stability is maintained for hours or even days before translation. In addition to oocytes and neurons, developing spermatids display significant uncoupling of transcription and translation for delayed translation. Therefore, spermiogenesis represents an excellent in vivo model for investigating the mechanism underlying uncoupled transcription and translation. Through full-length poly(A) deep sequencing, we discovered dynamic changes in poly(A) length through deadenylation and re-polyadenylation. Deadenylation appeared to be mediated by microRNAs (miRNAs), and transcripts with shorter poly(A) tails tend to be sequestered into ribonucleoprotein (RNP) granules for translational repression and stabilization. In contrast, re-polyadenylation might allow for translocation of the translationally repressed transcripts from RNP granules to polysomes. Overall, our data suggest that miRNA-dependent poly(A) length control represents a previously unreported mechanism underlying uncoupled translation and transcription in haploid male mouse germ cells.Entities:
Keywords: Adenylation; Alternative splicing; Deadenylation; Infertility; MicroRNA; Mouse; Poly(A) tail; Polysome; RNP; Spermiogenesis; Uncoupling of transcription and translation
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Year: 2022 PMID: 35588208 PMCID: PMC9270972 DOI: 10.1242/dev.199573
Source DB: PubMed Journal: Development ISSN: 0950-1991 Impact factor: 6.862