翻译与M1双链RNA增殖：MAK18 = RPL41B与放线菌酮消除
Translation and M1 double-stranded RNA propagation: MAK18 = RPL41B and cycloheximide curing.
作者信息
Carroll K, Wickner R B
机构信息
Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0830, USA.
出版信息
J Bacteriol. 1995 May;177(10):2887-91. doi: 10.1128/jb.177.10.2887-2891.1995.
Abstract
MAK18 is one of nearly 30 chromosomal genes of Saccharomyces cerevisiae necessary for propagation of the killer toxin-encoding M1 double-stranded RNA satellite of the L-A double-stranded RNA virus. We have cloned and sequenced MAK18 and find that it is identical to RPL41B, one of the two genes encoding large ribosomal subunit protein L41. The mak18-1 mutant is deficient in 60S subunits, which we suggest results in a preferential decrease in translation of viral poly(A)-deficient mRNA. We have reexamined the curing of M1 by low concentrations of cycloheximide (G. R. Fink and C. A. Styles, Proc. Natl. Acad. Sci. USA 69:2846-2849, 1972), which is known to act on ribosomal large subunit protein L29. We find that when M1 is supported by L-A proteins made from the poly(A)+ mRNA of a cDNA clone of L-A, cycloheximide does not decrease the M1 copy number, consistent with our hypothesis.
摘要
MAK18是酿酒酵母中近30个染色体基因之一，这些基因对于L-A双链RNA病毒的编码杀伤毒素的M1双链RNA卫星的繁殖是必需的。我们已经克隆并测序了MAK18，发现它与RPL41B相同，RPL41B是编码核糖体大亚基蛋白L41的两个基因之一。mak18-1突变体在60S亚基方面存在缺陷，我们认为这导致病毒多聚腺苷酸缺陷型mRNA的翻译优先减少。我们重新研究了低浓度环己酰亚胺对M1的消除作用（G. R. 芬克和C. A. 斯泰尔斯，《美国国家科学院院刊》69:2846 - 2849，1972），已知环己酰亚胺作用于核糖体大亚基蛋白L29。我们发现，当M1由来自L-A cDNA克隆的多聚腺苷酸加尾mRNA产生的L-A蛋白支持时，环己酰亚胺不会降低M1的拷贝数，这与我们的假设一致。
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