Abstract
We have examined the stability in vivo of three mutant species of trp mRNA which differ from wild type in the nature of their 5′-termini. These novel mRNA molecules originate from three mutationally generated promoters which lie within trp structural genes: trpE1423 lies near the carboxy-terminal end of trpE, trpD11 lies near the carboxy-terminal end of trpD (McPartland and Somerville, 1976) and trpC2121 lies near the center of trpC. When mRNA synthesis from the wild-type promoter is repressed by tryptophan, these strains still synthesize trp mRNA from their internal promoters at a relatively high efficiency in a constitutive fashion. The trp mRNA thus produced by the mutants lacks various lengths of the wild-type 5′-proximal RNA sequence. These shortened trp mRNA molecules decayed exponentially, at about the same rate as that of normal trp mRNA whose synthesis originates at the authentic trp promoter. Chloramphenicol inhibited the degradation of 5′-truncated trp mRNA fragments in a manner similar to that observed for wildtype trp mRNA, suggesting that the usual mechanism of mRNA decay is operative. We postulate that the initiation of mRNA decay at or near the 5′-end does not require some special nucleotide sequence; rather the 5′-proximal protion in general constitutes the target for nucleolytic attack.
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