The mechanism of recA polA lethality: Suppression by RecA-independent recombination repair activated by the lexA(Def) mutation in Escherichia coli

Journal Article · Sat Apr 01 04:00:00 EST 1995 · Genetics

OSTI ID:91159

Cao, Yang; Kogoma, Tokio ^[1]

---

1. Univ. of New Mexico Health Sciences Center, Albuquerque, NM (United States)

The mechanism of recA polA lethality in Escherichia coli has been studied. Complementation tests have indicated that both the 5{prime} {yields} 3{prime} exonuclease and the polymerization activities of DNA polymerase I are essential for viability in the absence of RecA protein, whereas the viability and DNA replication of DNA polymerase I-defective cells depend on the recombinase activity of RecA. An alkaline sucrose gradient sedimentation analysis has indicated that RecA has only a minor role in Okazaki fragment processing. Double-strand break repair is proposed for the major role of RecA in the absence of DNA polymerase I. The lexA(Def)::Tn5 mutation has previously been shown to suppress the temperature-sensitive growth of recA200(Ts) polA25::spc mutants. The lexA(Def) mutation can alleviate impaired DNA synthesis in the recA200(Ts) polA25::spc mutant cells at the restrictive temperature. recF{sup +} is essential for this suppression pathway, recJ and recQ mutations have minor but significant adverse effects on the suppression. The recA200(Ts) allele in the recA200(Ts) polA25::spc lexA(Def) mutant can be replaced by {Delta}recA, indicating that the lexA(Def)-induced suppression is RecA independent. lexA(Def) reduces the sensitivity of {Delta}recA polA25::spc cells to UV damage by {approximately}10{sup 4}-fold. lexA(Def) also restores P1 transduction proficiency to the {Delta}recA polA25::spc mutant to a level that is 7.3% of the recA{sup +} wild type. These results suggest that lexA(Def) activates a RecA-independent, RecF-dependent recombination repair pathway that suppresses the defect in DNA replication in recA polA double mutants. 52 refs., 7 figs., 5 tabs.

• OSTI ID: 91159
• Journal Information: Genetics, Journal Name: Genetics Journal Issue: 4 Vol. 139; ISSN GENTAE; ISSN 0016-6731
• Country of Publication: United States
• Language: English

Related Subjects

55 BIOLOGY AND MEDICINE
BASIC STUDIES
ANIMAL CELLS
DNA HYBRIDIZATION
DNA POLYMERASES
DNA REPLICATION
ENZYMES
ESCHERICHIA COLI
GENE MUTATIONS
GENE RECOMBINATION
GENES
GENETIC RADIATION EFFECTS
GROWTH
LETHAL MUTATIONS
PLASMIDS
PROTEINS
SENSITIVITY
TEMPERATURE DEPENDENCE
ULTRAVIOLET RADIATION