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噬菌体T4的rII基因突变抑制子影响启动子的利用。

Suppressors of mutations in the rII gene of bacteriophage T4 affect promoter utilization.

作者信息

Hall D H, Snyder R D

出版信息

Genetics. 1981 Jan;97(1):1-9. doi: 10.1093/genetics/97.1.1.

DOI:10.1093/genetics/97.1.1
PMID:7262547
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1214376/
Abstract

Homyk, Rodriguez and Weil (1976) have described T4 mutants, called sip, that partially suppress the inability of T4rII mutants to grow in lambda lysogens. We have found that mutants sip1 and sip2 are resistant to folate analogs and overproduce FH2 reductase. The results of recombination and complementation studies indicate that sip mutations are in the mot gene. Like other mot mutations (Mattson, Richardson and Goodin 1974; Chace and Hall 1975; Sauerbier, Hercules and Hall 1976), the sip2 mutation affects the expression of many genes and appears to affect promoter utilization. The mot gene function is not required for T4 growth on most hosts, but we have found that it is required for good growth on E. coli CTr5X. Homyk, Rodriguez and Weil (1976) also described L mutations that reverse the effects of sip mutations. L2 decreases the folate analog resistant and the inability of sip2 to grow on CTr5X. L2 itself is partially resistant to a folate analog, and appears to reverse the effects of sip2 on gene expression. These results suggest that L2 affects another regulatory gene related to the mot gene.

摘要

霍米克、罗德里格斯和韦尔(1976年)描述了一种名为sip的T4突变体,它能部分抑制T4 rII突变体在λ溶原菌中生长的无能状态。我们发现突变体sip1和sip2对叶酸类似物具有抗性,并且过量产生FH2还原酶。重组和互补研究结果表明,sip突变存在于mot基因中。与其他mot突变(马特森、理查森和古丁,1974年;蔡斯和霍尔,1975年;索尔比尔、赫尔克里士和霍尔,1976年)一样,sip2突变影响许多基因的表达,并且似乎影响启动子的利用。在大多数宿主上,T4生长不需要mot基因功能,但我们发现,在大肠杆菌CTr5X上良好生长需要该基因。霍米克、罗德里格斯和韦尔(1976年)还描述了L突变,这些突变可逆转sip突变的影响。L2降低了叶酸类似物抗性以及sip2在CTr5X上生长的无能状态。L2本身对一种叶酸类似物具有部分抗性,并且似乎逆转了sip2对基因表达的影响。这些结果表明,L2影响另一个与mot基因相关的调控基因。

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本文引用的文献

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