Mr, identified a novel gene of bacteriophage T4, gene 61.5, which appe
ars to be involved in protein synthesis late in infection. Northern bl
ot analysis revealed that a mutant of 61.5 accumulated truncated trans
cripts of representative late genes. Using a double mutant of genes 61
.5 and 55, which prevents transcription of late genes, we demonstrate
that even transcripts of middle genes, while full-length when initiall
y expressed, are similarly truncated at later stages of infection. The
se results indicate that the abnormality in transcript length occurs l
ate in infection, regardless of whether the transcript derives from a
middle or a late gene. Primer-extension analysis revealed that the 5'
ends of the late gene 23 transcripts that accumulated in gene 61.5 mut
ant-infected cells were located at internal discrete sites as well as
at the expected transcription start site. Moreover, the decay rates of
full-length transcripts from genes uvsY or 45 were more than twofold
faster in the absence of a functional gene 61.5. These results suggest
that mutation of gene 61.5 activates endonucleolytic cleavage of midd
le and late transcripts, probably by RNase M.