Abstract：
:Gene duplication is a major evolutionary force driving adaptation and speciation, as it allows for the acquisition of new functions and can augment or diversify existing functions. Here, we report a gene duplication event that yielded another outcome--the generation of antagonistic functions. One product of this duplication event--UPF3B--is critical for the nonsense-mediated RNA decay (NMD) pathway, while its autosomal counterpart--UPF3A--encodes an enigmatic protein previously shown to have trace NMD activity. Using loss-of-function approaches in vitro and in vivo, we discovered that UPF3A acts primarily as a potent NMD inhibitor that stabilizes hundreds of transcripts. Evidence suggests that UPF3A acquired repressor activity through simple impairment of a critical domain, a rapid mechanism that may have been widely used in evolution. Mice conditionally lacking UPF3A exhibit "hyper" NMD and display defects in embryogenesis and gametogenesis. Our results support a model in which UPF3A serves as a molecular rheostat that directs developmental events.
journal_name
Celljournal_title
Cellauthors
Shum EY,Jones SH,Shao A,Dumdie J,Krause MD,Chan WK,Lou CH,Espinoza JL,Song HW,Phan MH,Ramaiah M,Huang L,McCarrey JR,Peterson KJ,De Rooij DG,Cook-Andersen H,Wilkinson MFdoi
10.1016/j.cell.2016.02.046subject
Has Abstractpub_date
2016-04-07 00:00:00pages
382-95issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(16)30196-9journal_volume
165pub_type
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