Isolation and characterization of herC, a mutation of Escherichia coli affecting maintenance of ColE1 |
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| Authors: | Koichi Kawakami Satoshi Naito Naoki Inoue Yoshikazu Nakamura Hideo Ikeda and Hisao Uchida |
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| Institution: | (1) The Institute of Medical Science, The University of Tokyo, 108 P.O. Takanawa, Tokyo, Japan;(2) Present address: Molecular Genetics Research Laboratory, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, 113 Tokyo, Japan;(3) Present address: Department of Virology and Rickettsiology, The National Institute of Health, 2-10-35 Kamiosaki, Shinagawaku, 141 Tokyo, Japan;(4) Present address: Department of Biosciences, Teikyo University, 320 Nagaoka-cho, Utsunomiya, Japan |
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| Abstract: | Summary Two modes of ColE1 DNA replication are known, one dependent on RNase H, and the other RNase H independent. The cer114 mutant of the ColE1 replicon is defective in both modes and carries a single base pair alteration 95 by upstream of the replication origin. An Escherichia coli mutant which restored maintenance of the cer114 replicon was isolated. This host suppressor mutant is defective in RNase H and carries a herC, mutation located at 62 min of the E. coli chromosome. The herC, mutation is recessive to its wild-type allele and supports maintenance of the mutant replicon in the absence of RNase H. The herC, mutation alone conferred cold-sensitive growth, suggesting that the herC, gene product is essential for cell growth. The 1832 by E. coli DNA fragment, containing the wild-type allele of the herC, mutation, was cloned and an open reading frame for the HerC protein was determined. |
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| Keywords: | ColE1 replication Primer RNA Suppressor mutation RF2 Ribonuclease H |
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