Defects in the mRNA export factors Rat7p Gle1p Mex67p and Rat8p cause hyperadenylation during 3-end formation of nascent transcripts.

摘要

The biosynthesis and function of eukaryotic mRNAs requires a series of events including nuclear polyadenylation, transport to the cytoplasm, translation, and ultimately mRNA degradation. To identify the interrelationships between these events, we examined the synthesis and fate of mRNAs in several strains defective in mRNA export. Strains carrying lesions in RAT7, GLE1, MEX67, and RAT8, produce nascent transcripts carrying poly(A) tails roughly 30 residues longer than the nascent poly(A) tails observed in wild type. In the rat7-1, rat8-2, and mex67-5 strains, the hyperadenylated transcripts undergo a novel form of deadenylation to chase into a population with normal poly(A) tail lengths, which cofractionate with polysomes, undergo nonsense-mediated decay, and are degraded by the normal cytoplasmic decay machinery. This suggests a relationship between the mechanism of processing to a normal poly(A) tail length and the ability of these transcripts to proceed in their metabolism. These observations provide further support for the view that mRNA 3'-end formation and mRNA export are mechanistically coupled events.