Kao S H, McClain W H
J Virol. 1980 Apr;34(1):104-7. doi: 10.1128/JVI.34.1.104-107.1980.
Previous studies indicated that (i) T4 gene s product (gps) protects infected cells from superinfection lysis from without, (ii) the absence of gps in infected cells also leads to lysis from within even when T4 e lysozyme is absent, (iii) T4 gene 5 product (gp5), a polypeptide of the virion baseplate, may be responsible for inducing lysis from without, and (iv) altered gp5 of the T4 mutant 5ts1 can replace e lysozyme to cause lysis from within. Results of this study showed that (i) wild-type gp5 in infected cells lacking e lysozyme was responsible for lysis from within in the absence of gps, and (ii) gps did not protect infected cells from superinfection lysis from without by 5ts1 phage. We prpose that gps normally prevents functional expression of wild-type gp5 activity from either side of the cell wall, whereas the 5ts1 form of gp5 is insensitive to the gps barrier and induces lysis from either side of the cell wall.
(i)T4基因s产物(gps)可保护受感染细胞免受外部超感染裂解;(ii)即使不存在T4 e溶菌酶,受感染细胞中gps的缺失也会导致内部裂解;(iii)T4基因5产物(gp5),一种病毒粒子基板的多肽,可能负责诱导外部裂解;(iv)T4突变体5ts1的改变的gp5可以替代e溶菌酶导致内部裂解。本研究结果表明:(i)在缺乏e溶菌酶的受感染细胞中,野生型gp5在不存在gps的情况下负责内部裂解;(ii)gps不能保护受感染细胞免受5ts1噬菌体的外部超感染裂解。我们推测,gps通常可防止野生型gp5活性在细胞壁两侧的功能性表达,而gp5的5ts1形式对gps屏障不敏感,并可诱导细胞壁两侧的裂解。