Cold-induced protein RBM3 orchestrates neurogenesis via modulating Yap mRNA stability in cold stress

In mammals, a constant body temperature is an important basis for maintaining life activities. Here, we show that when pregnant mice are subjected to cold stress, the expression of RBM3, a cold-induced protein, is increased in the embryonic brain. When RBM3 is knocked down or knocked out in cold str...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of cell biology Vol. 217; no. 10; pp. 3464 - 3479
Main Authors Xia, Wenlong, Su, Libo, Jiao, Jianwei
Format Journal Article
LanguageEnglish
Published United States Rockefeller University Press 01.10.2018
Subjects
3' Untranslated Regions
Adaptor Proteins, Signal Transducing - biosynthesis
Adaptor Proteins, Signal Transducing - genetics
Animals
Binding sites
Body temperature
Brain
Brain - embryology
Cell Cycle Proteins
Change detection
Cold
Cold-Shock Response
Embryo, Mammalian - embryology
Embryogenesis
Gene expression
Gene Expression Regulation, Developmental
Mice
Mice, Inbred ICR
Mice, Knockout
mRNA stability
Neurogenesis
Nucleotide Motifs
Phosphoproteins - biosynthesis
Phosphoproteins - genetics
Protein expression
Proteins
Ribonucleic acid
RNA
RNA Stability
RNA-Binding Proteins - genetics
RNA-Binding Proteins - metabolism
Rodents
Stability
Stress
Stresses
Temperature effects
Yes-associated protein
Online AccessGet full text

Cover

More Information
Summary:In mammals, a constant body temperature is an important basis for maintaining life activities. Here, we show that when pregnant mice are subjected to cold stress, the expression of RBM3, a cold-induced protein, is increased in the embryonic brain. When RBM3 is knocked down or knocked out in cold stress, embryonic brain development is more seriously affected, exhibiting abnormal neuronal differentiation. By detecting the change in mRNA expression during maternal cold stress, we demonstrate that Yap and its downstream molecules are altered at the RNA level. By analyzing RNA-binding motif of RBM3, we find that there are seven binding sites in 3'UTR region of Yap1 mRNA. Mechanistically, RBM3 binds to Yap1-3'UTR, regulates its stability, and affects the expression of YAP1. RBM3 and YAP1 overexpression can partially rescue the brain development defect caused by RBM3 knockout in cold stress. Collectively, our data demonstrate that cold temperature affects brain development, and RBM3 acts as a key protective regulator in cold stress.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0021-9525
1540-8140
DOI:10.1083/JCB.201801143