Chattoraj Partho, Ganguly Tridib, Nandy Ranjan Kumar, Sau Subrata
Department of Biochemistry, Bose Institute, CIT Scheme VII M, Calcutta, India.
BMB Rep. 2008 May 31;41(5):363-8. doi: 10.5483/bmbrep.2008.41.5.363.
Two genes of temperate mycobacteriophage L5, namely, gp63 and gp64, were hypothesized to be toxic to M. smegmatis. An identical L5 gp64 ortholog (designated hlg1) was cloned from homoimmune mycobacteriophage L1 and characterized at length here. As expected, hlg1 affected the growth of M. smegmatis when overexpressed from a resident plasmid. HLG1 (the protein encoded by hlg1) in fact caused growth retardation of M. smegmatis and the region encompassing its 57-114 C-terminal amino acid residues was found indispensable for its growth-retardation activity. Both nucleic acid and protein biosynthesis were severely impaired in M. smegmatis expressing HLG1. Interestingly, HLG1 also affected E. coli almost similarly. This putative delayed early lipoprotein did not participate in the lytic growth of L1.
推测温和型分枝杆菌噬菌体L5的两个基因,即gp63和gp64,对耻垢分枝杆菌有毒性。从同免疫分枝杆菌噬菌体L1中克隆出一个相同的L5 gp64直系同源基因(命名为hlg1),并在此进行了详细表征。正如预期的那样,当从驻留质粒中过表达时,hlg1影响了耻垢分枝杆菌的生长。事实上,HLG1(由hlg1编码的蛋白质)导致耻垢分枝杆菌生长迟缓,并且发现包含其57 - 114个C末端氨基酸残基的区域对其生长迟缓活性是必不可少的。在表达HLG1的耻垢分枝杆菌中,核酸和蛋白质生物合成均受到严重损害。有趣的是,HLG1对大肠杆菌的影响几乎类似。这种假定的延迟早期脂蛋白不参与L1的裂解生长。