Suppr超能文献

噬菌体T1指定的基因位点与多肽的相关性。

Correlation of genetic loci and polypeptides specified by bacteriophage T1.

作者信息

Ritchie D A, Joicey D H, Martin D T

出版信息

J Gen Virol. 1983 Jun;64 (Pt 6):1355-63. doi: 10.1099/0022-1317-64-6-1355.

Abstract

The effects of amber mutations in the 24 known essential genes of phage T1 on phage-directed protein synthesis were examined by SDS-polyacrylamide gel electrophoresis of radiolabelled polypeptides from infected non-permissive cells. Mutations in nine genes (genes 1, 2, 3, 3.5, 5, 7-8, 10, 13.3 and 15) each resulted in the failure to synthesize a single polypeptide. Since the synthesis of each of these polypeptides was at least partially restored in permissive infections and wholly restored in am+ revertant infections we conclude that the affected polypeptide is the primary gene product. Mutations in genes 13.7, 16 and 17, which are required for head formation, are all defective in the synthesis of a 68000 mol. wt. non-structural polypeptide. Mutants in the head genes 13 and 14 fail to cleave P7p to P7, the major structural component of proheads. Gene 14 mutants also fail to make a 45000 mol. wt. non-structural polypeptide which appears to be involved with the gene 13 product in the P7p cleavage reaction. The protein products of the DNA genes 1, 2 and 3.5 are, as expected, synthesized predominantly early in infection whereas those of the remainder, which determine head and tail formation, are made in greater amounts late in infection. Gene 3, a tail gene which has been mapped within the 'early' DNA gene cluster, codes for a 75000 mol. wt. polypeptide synthesized predominantly late in infection. This observation suggests that the early genes 1, 2, 3.5 and 4 do not form an operon under the control of a single early promoter.

摘要

通过对来自受感染非允许细胞的放射性标记多肽进行SDS-聚丙烯酰胺凝胶电泳,研究了噬菌体T1的24个已知必需基因中的琥珀突变对噬菌体指导的蛋白质合成的影响。九个基因(基因1、2、3、3.5、5、7 - 8、10、13.3和15)中的突变各自导致无法合成单一多肽。由于这些多肽中的每一种的合成在允许感染中至少部分恢复,并且在am +回复突变感染中完全恢复,我们得出结论,受影响的多肽是主要基因产物。头部形成所需的基因13.7、16和17中的突变,在合成68000摩尔质量的非结构多肽方面均有缺陷。头部基因13和14中的突变体无法将P7p切割成原头部的主要结构成分P7。基因14突变体也无法合成一种45000摩尔质量的非结构多肽,该多肽似乎在P7p切割反应中与基因13产物一起起作用。正如预期的那样,DNA基因1、2和3.5的蛋白质产物在感染早期主要合成,而其余决定头部和尾部形成的基因的产物在感染后期合成量更大。基因3是一个尾部基因,已定位在“早期”DNA基因簇内,编码一种75000摩尔质量的多肽,主要在感染后期合成。这一观察结果表明,早期基因1、2、3.5和4在单个早期启动子的控制下不形成操纵子。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验