Postreplication repair and its inhibition by chloramphenicol and caffeine, as seen in alkaline sucrose gradients, were compared between a uv non-mutable strain uvrA- umuC- and normally mutable strains uvrA- recF- and uvrA- umu+rec+ of Escherichia coli K-12. The uvrA- umuC- strain performed postrepli
The dependence of postreplication repair on uvrB in a recF mutant of Escherichia coli K-12
β Scribed by Rothman, Robert H. ;Clark, Alvin J.
- Publisher
- Springer
- Year
- 1977
- Tongue
- English
- Weight
- 660 KB
- Volume
- 155
- Category
- Article
- ISSN
- 0026-8925
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β¦ Synopsis
Mutants carrying recF143 or recF144 show wild type levels of host cell reactivation of UV-irradiated lambdavir and wild type rates of excision gap closure in repairing UV damage to their own DNA. The same mutants showed reduced rates of postreplication repair strand joining. When uvrA- recF- or uvrB- recF- strains are tested, postreplication repair strand joining is incomplete or does not occur at fluences above 1 J/m2. We suggest that there may be a UvrAB and a RecF pathway of postreplication repair or that the repair functions controlled or determined by uvrA uvrB and by recF may be similar. An intermediate in postreplication repair may accumulate in the uvr- recF- strain.
π SIMILAR VOLUMES
W-reactivation is reduced by recF143 and recF144 mutations and is undetectable if a second mutation at either the uvrA or uvrB locus is combined with recF143. The uvrA and uvrB mutations alone block W-reactivation partially. A reeL152 mutation also partially blocks W-reactivation by itself. In combi
The mutation recL152 leads to a reduction of excision repair as measured by an increase in the time required to close uvrA uvrB dependent incision breaks, and by a reduction of host cell reactivation ability. Postreplication repair is also delayed when measured in a uvrB5 recL152 double mutant. Such