Towards the mechanism(s) of YB-3 synthesis regulation by YB-1

RNA Biol. 2021 Nov;18(11):1630-1641. doi: 10.1080/15476286.2020.1859243. Epub 2020 Dec 27.

Abstract

Y-box binding proteins are members of the family of proteins containing the evolutionarily conserved cold shock domain. Their cellular functions are quite diverse, including transcription and translation regulation, participation in pre-mRNA splicing, mRNA stabilization and packaging into mRNPs, involvement in DNA repair, and some others. To date, we know little about the plausible functional interchangeability of Y-box binding proteins. Our previous finding was that in YB-1-null HEK293T cells the synthesis of YB-3 is enhanced, thus enabling YB-3 to interact with a larger set of mRNAs and compensate for the YB-1 absence. We suggested the existence of a mechanism of YB-3 synthesis regulation by its paralog, YB-1. Here we demonstrate that YB-1 participates in the translational control and stabilization of YB-3 mRNA through untranslated regions of YB-3 mRNA.

Keywords: YB-1; YB-3; YBX1; YBX3; mRNA stability; translational control.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CCAAT-Enhancer-Binding Proteins / genetics
  • CCAAT-Enhancer-Binding Proteins / metabolism*
  • Gene Expression Regulation*
  • HEK293 Cells
  • Humans
  • Protein Binding
  • Protein Biosynthesis*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism*
  • Ribonucleoproteins / genetics
  • Ribonucleoproteins / metabolism*
  • Y-Box-Binding Protein 1 / genetics
  • Y-Box-Binding Protein 1 / metabolism*

Substances

  • CCAAT-Enhancer-Binding Proteins
  • RNA, Messenger
  • Ribonucleoproteins
  • Y-Box-Binding Protein 1
  • YBX1 protein, human
  • messenger ribonucleoprotein

Grants and funding

This work was supported by the Russian Foundation for Basic Research (# 18-04-00595) and the Russian Science Foundation (# 19-74-20129) [section ‘In the absence of YB-1, the stability of YB-3 mRNA decreases’]. The publication fee is funded by the Russian Science Foundation (# 19-74-20129).