DNA repair in Haemophilus influenzae appears to be quite different from that seen in Escherichia coli in that H. influenzae shows neither "S.O.S." nor "adaptation" phenomena. Repair of DNA lesions in H. influenzae has been seen to occur via recombinational, excision, and mismatch repair pathways acting independently of one another. I have isolated an ultraviolet (UV)-sensitive mutator mutant (mutB1) of H. influenzae Rd which shows deficiencies in both recombinational and mismatch repair pathways. This mutant is sensitive to a variety of DNA damaging agents as well as being hypermutable by alkylating agents and base analogues. MutB1 cells do not show post-UV DNA breakdown but do begin excision after UV irradiation. / Genetic transformation with UV-irradiated DNA on mutB1 recipients shows that high (HE) and low (LE) efficiency markers are transformed at a ratio of 1.0 as in the mismatch repair deficient hex1 mutant; however, kinetics of UV-inactivation experiments indicate that HE markers are sensitized and act as LE markers do on wild type recipients. Thus, the mutB gene product appears to play a role in both DNA repair and genetic transformation. / An E. coli mutant (uvrD) having many similar properties to the mutB1 mutant has recently been shown deficient in DNA helicase II. A model is outlined which presents a role for a DNA helicase in both DNA repair and genetic transformation of H. influenzae. / Source: Dissertation Abstracts International, Volume: 46-10, Section: B, page: 3333. / Thesis (Ph.D.)--The Florida State University, 1985.
| Identifer | oai:union.ndltd.org:fsu.edu/oai:fsu.digital.flvc.org:fsu_75680 |
| Contributors | WALTER, RONALD BRUCE., Florida State University |
| Source Sets | Florida State University |
| Detected Language | English |
| Type | Text |
| Format | 187 p. |
| Rights | On campus use only. |
| Relation | Dissertation Abstracts International |
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