한빛사 논문
Jungyun Park1,5, Jwa-Won Seo2,5, Narae Ahn1, Seokju Park2, Jungwook Hwang1,3,* & Jin-Wu Nam2,4,*
1 Graduate School for Biomedical Science & Engineering, Hanyang University, Seoul, Republic of Korea. 2 Department of Life Science, College of Natural Sciences, Hanyang University, Seoul, Republic of Korea. 3 Department of Medical Genetics, College of Medicine, Hanyang University, Seoul, Republic of Korea. 4 Research Institute for Convergence of Basic Sciences, Hanyang University, Seoul, Republic of Korea. 5 These authors contributed equally: Jungyun Park, Jwa-Won Seo.
*Correspondence and requests for materials should be addressed to J.H. or to J.-W.N.
Abstract
The stability and quality of metazoan mRNAs are under microRNA (miRNA)-mediated and nonsense-mediated control. Although UPF1, a core mediator of nonsense-mediated mRNA decay (NMD), mediates the decay of target mRNA in a 3′UTR-length-dependent manner, the detailed mechanism remains unclear. Here, we suggest that 3′UTR-length-dependent mRNA decay is not mediated by nonsense mRNAs but rather by miRNAs that downregulate target mRNAs via Ago-associated UPF1/SMG7. Global analyses of mRNAs in response to UPF1 RNA interference in miRNA-deficient cells reveal that 3′UTR-length-dependent mRNA decay by UPF1 requires canonical miRNA targeting. The destabilization of miRNA targets is accomplished by the combination of Ago2 and UPF1/SMG7, which may recruit the CCR4-NOT deadenylase complex. Indeed, loss of the SMG7-deadenylase complex interaction increases the levels of transcripts regulated by UPF1-SMG7. This UPF1/SMG7-dependent miRNA-mediated mRNA decay pathway may enable miRNA targeting to become more predictable and expand the miRNA-mRNA regulatory network.
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