Genetic complementation by cloned bacteriophage T4 late genes.

1981 ◽  
Vol 39 (1) ◽  
pp. 31-45 ◽  
Author(s):  
K A Jacobs ◽  
L M Albright ◽  
D K Shibata ◽  
E P Geiduschek
Genetics ◽  
2002 ◽  
Vol 160 (1) ◽  
pp. 5-12
Author(s):  
Toshie Kai ◽  
Tetsuro Yonesaki

Abstract The dmd gene of bacteriophage T4 is required for regulation of mRNA stability in a stage-dependent manner during infection. When this gene is mutated, late genes are globally silenced because of rapid degradation of mRNAs. To investigate the mechanism of such mRNA degradation, we analyzed the late gene soc transcripts. The degradation of soc mRNA was remarkably stabilized when its ability to be translated was impaired; either disruption of translation initiation signals or elimination of termination codons was effective in stabilization of soc mRNA and removal of elongation modestly stabilized it. Even in the absence of translation, however, the residual activity was still significant. These results suggested that the degradation of soc transcripts was promoted by two different mechanisms; one is dependent on translation and the other independent of translation. We found several cleavages introduced into soc RNA specifically when the dmd gene was mutated; some of them could be linked to polypeptide chain elongation and termination, suggesting the correlation with ribosomal action, and the others were independent of translation.


1970 ◽  
Vol 53 (1) ◽  
pp. 69-89 ◽  
Author(s):  
Robert Bruner ◽  
Ronald E. Cape
Keyword(s):  

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 7-14 ◽  
Author(s):  
Toshie Kai ◽  
Harold E Selick ◽  
Tetsuro Yonesaki

Abstract We identified a novel gene of bacteriophage T4, gene 61.5, which appears to be involved in protein synthesis late in infection. Northern blot analysis revealed that a mutant of 61.5 accumulated truncated transcripts 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 initially expressed, are similarly truncated at later stages of infection. These results indicate that the abnormality in transcript length occurs late 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 mutant-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 middle and late transcripts, probably by RNase M.


Genetics ◽  
2001 ◽  
Vol 158 (1) ◽  
pp. 7-17 ◽  
Author(s):  
Hiroyuki Ueno ◽  
Tetsuro Yonesaki

Abstract Gene 61.5 of bacteriophage T4 has a unique role in gene expression. When this gene is mutated, mRNAs of many late genes are rapidly degraded, resulting in late-gene silencing. Here, we characterize an extragenic suppressor, ssf5, of a gene 61.5 mutation. ssf5 was found to be an amber mutation in motA, which encodes a transcription activator for T4 middle genes. When this gene is mutated, both degradation and specific cleavage of late-gene mRNA is induced after a delay, as exemplified by soc mRNA. Consequently, partial late-gene expression occurs. In an ssf5 genetic background, a gene 61.5 mutation exhibits a novel phenotype: in contrast to late-gene mRNA, middle-gene mRNA is stabilized and the expression of middle genes is prolonged. This is attributable to an activity of gene 61.5 specific for degradation of middle-gene mRNA. The degradation of middle-gene mRNA in the presence of a normal gene 61.5 appears in parallel with the degradation of late-gene mRNA in its absence. This observation suggests that the mRNA-degrading activity that silences late genes in cells infected with a gene 61.5 mutant is targeted to middle-gene mRNA when gene 61.5 is wild type. These results and the results obtained in the presence of a normal motA gene suggest that gene 61.5 protein functions to discriminate mRNAs for degradation in a stage-dependent manner.


Author(s):  
Fred Eiserling ◽  
A. H. Doermann ◽  
Linde Boehner

The control of form or shape inheritance can be approached by studying the morphogenesis of bacterial viruses. Shape variants of bacteriophage T4 with altered protein shell (capsid) size and nucleic acid (DNA) content have been found by electron microscopy, and a mutant (E920g in gene 66) controlling head size has been described. This mutant produces short-headed particles which contain 2/3 the normal DNA content and which are non-viable when only one particle infects a cell (Fig. 1).We report here the isolation of a new mutant (191c) which also appears to be in gene 66 but at a site distinct from E920g. The most striking phenotype of the mutant is the production of about 10% of the phage yield as “giant” virus particles, from 3 to 8 times longer than normal phage (Fig. 2).


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