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

The biosynthesis and function of eukaryotic mRNAs requires a series of even ts including nuclear polyadenylation, transport to the cytoplasm, translati on, and ultimately mRNA degradation. To identify the interrelationships bet ween these events, we examined the synthesis and fate of mRNAs in several s trains defective in mRNA export. Strains carrying lesions in RAT7, GLE1, ME X67, and RAT8, produce nascent transcripts carrying poly(A) tails roughly 3 0 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 un dergo 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 norm al poly(A) tail length and the ability of these transcripts to proceed in t heir metabolism. These observations provide further support for the view th at mRNA 3'-end formation and mRNA export are mechanistically coupled events .