Cellular stress alters 3′UTR landscape through alternative polyadenylation and isoform-specific degradation

Dinghai Zheng, Ruijia Wang, Qingbao Ding, Tianying Wang, Bingning Xie, Lu Wei, Zhaohua Zhong and Bin Tian ()
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Dinghai Zheng: Rutgers New Jersey Medical School
Ruijia Wang: Rutgers New Jersey Medical School
Qingbao Ding: Rutgers New Jersey Medical School
Tianying Wang: Harbin Medical University
Bingning Xie: Rutgers New Jersey Medical School
Lu Wei: Rutgers New Jersey Medical School
Zhaohua Zhong: Harbin Medical University
Bin Tian: Rutgers New Jersey Medical School

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Most eukaryotic genes express alternative polyadenylation (APA) isoforms with different 3′UTR lengths, production of which is influenced by cellular conditions. Here, we show that arsenic stress elicits global shortening of 3′UTRs through preferential usage of proximal polyadenylation sites during stress and enhanced degradation of long 3′UTR isoforms during recovery. We demonstrate that RNA-binding protein TIA1 preferentially interacts with alternative 3′UTR sequences through U-rich motifs, correlating with stress granule association and mRNA decay of long 3′UTR isoforms. By contrast, genes with shortened 3′UTRs due to stress-induced APA can evade mRNA clearance and maintain transcript abundance post stress. Furthermore, we show that stress causes distinct 3′UTR size changes in proliferating and differentiated cells, highlighting its context-specific impacts on the 3′UTR landscape. Together, our data reveal a global, 3′UTR-based mRNA stability control in stressed cells and indicate that APA can function as an adaptive mechanism to preserve mRNAs in response to stress.

Date: 2018
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DOI: 10.1038/s41467-018-04730-7

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