Modulation of bacteriophage T4 capsid size

被引:11
作者
Haynes, JA
Eiserling, FA
机构
[1] UNIV CALIF LOS ANGELES,DEPT MICROBIOL & MOLEC GENET,LOS ANGELES,CA 90095
[2] UNIV CALIF LOS ANGELES,INST MOLEC BIOL,LOS ANGELES,CA 90095
关键词
D O I
10.1006/viro.1996.0353
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Bacteriophage T4 capsid assembly requires the vertex protein (gp24). Mutations that bypass this requirement are found in gene 23, which produces the major capsid protein (gp23). The latter were used to study the role of gp24 in head length control. We found that gp24 is no longer present in the capsids of several gp24 bypass mutants. We measured the capsid lengths of several of these bypass mutants, because gp24 had been reported to be implicated in headlength control. One bypass mutant (reported in 1977) produced 40-60% short headed (''petite'') phage in the presence of wild-type amounts of gp24. The bypass mutations, when combined with amber mutations in gene 24, produced normal size heads in either suppressor or nonsuppressor host bacteria. When several known bypass mutations were back-crossed with wild-type phage, one-third of the byp/24wt mutants isolated produced large amounts of petite phage, indicating that the ability to produce petite phage is a general properly of the bypass mutations. Sequencing several of these bypass mutants showed that those that produced petite phage contained at least one additional missense mutation in gene 23. This suggests that gp24 itself has no direct role in head length regulation, but that in the presence of bypass 24 mutations and certain easily acquired gene 23 mutations (called trb) the gp23-gp24 interactions can modulate head length. (C) 1996 Academic Press, Inc.
引用
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页码:67 / 77
页数:11
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