SMG-1 is a phosphatidylinositol kinase-related protein kinase required for nonsense-mediated mRNA decay in Caenorhabditis elegans

被引：91

作者：

Grimson, A ^{[1
]}

O'Connor, S ^{[1
]}

Newman, CL ^{[1
]}

Anderson, P ^{[1
]}

机构：

[1] Univ Wisconsin, Dept Genet, Madison, WI 53706 USA

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2004年 / 24卷 / 17期

关键词：

D O I：

10.1128/MCB.24.17.7483-7490.2004

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Eukaryotic messenger RNAs containing premature stop codons are selectively and rapidly degraded, a phenomenon termed nonsense-mediated mRNA decay (NMD). Previous studies with both Caenohabditis elegans and mammalian cells indicate that SMG-2/human UPF1, a central regulator of NMD, is phosphorylated in an SMG-1-dependent manner. We report here that smg-1, which is required for NMD in C. elegans, encodes a protein kinase of the phosphatidylinositol kinase superfamily of protein kinases. We identify null alleles of smg-1 and demonstrate that SMG-1 kinase activity is required in vivo for NMD and in vitro for SMG-2 phosphorylation. SMG-1 and SMG-2 coimmunoprecipitate from crude extracts, and this interaction is maintained in smg-3 and smg-4 mutants, both of which are required for SMG-2 phosphorylation in vivo and in vitro. SMG-2 is located diffusely through the cytoplasm, and its location is unaltered in mutants that disrupt the cycle of SMG-2 phosphorylation. We discuss the role of SMG-2 phosphorylation in NMD.

引用

页码：7483 / 7490

页数：8

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[11] A REGULATORY MECHANISM THAT DETECTS PREMATURE NONSENSE CODONS IN T-CELL RECEPTOR TRANSCRIPTS IN-VIVO IS REVERSED BY PROTEIN-SYNTHESIS INHIBITORS IN-VITRO [J].