# REGULATION OF SOS FUNCTIONS IN ESCHERICHIA COLI

> **NIH NIH R01** · RUTGERS, THE STATE UNIV OF N.J. · 1989 · $168,807

## Abstract

The long-term goal of the proposed research is to understand fully the
mutagenic activity (SOS mutagenesis) induced in E. coli in response to
radiations and carcinogenic chemicals as part of a more complex response
(the SOS response) to genetic damage.  LexA protein is the common repressor
of at least 17 SOS genes, which are derepressed when RecA protein is
activated by DNA damage to a form (RecA*) that can cause proteolytic
cleavage of LexA.  Activated RecA* has an additional essential role in SOS
mutagenesis, distinct from cleavage of LexA or any other repressor.  The
additional activity could be either proteolytic processing of one or more
other proteins or a mechanistic function possible only in the activated
state.  As an approach to identification of this unknown RecA* role, a
mutant allele, recA730, that causes constitutive hyperactivity of RecA*,
will be cloned, RecA730 protein purified, and its activity in an in vitro
assay for cleavage of LexA compared with that of RecA+ and other mutant
RecA proteins.  Another mutant allele, recA718, which causes UV sensitivity
and UV hypermutability, will also be cloned and its protein product
purified and partially characterized.  Both RecA730 and RecA718 will be
made available to laboratories investigating RecA protein activities in
various in vitro systems.  The following additional investigations, all
relating to aspects of SOS mutagenesis not well understood, are also
proposed:  1) determination of the basis of the mutator activity caused by
plasmid pKM101 that differs from SOS mutator activity in several ways,
e.g., it is expressed in lexA(Ind-) strains and is enhanced by low
temperatures; 2) testing of the hypothesis that SOS mutator activity
involves inhibition of the proofreading activity of DNA polymerase III, by
examining the interaction of mutD(dnaQ) alleles (which are known to inhibit
Pol III proofreading) with recA730, which causes constitutive SOS mutator
activity; 3) determination of the basis of the high frequency of novel recA
alleles recovered in crosses of K12 recA441 donors x B/r recA+ recipients,
and 4) reexamination of the phenomenon known as "mutation frequency
decline" (MFD) to test the hypothesis that it is caused by medium-dependent
changes in DNA conformation that affect repair of UV photoproducts at
specific sites in certain tRNA genes.  A deeper understanding of the events
leading from DNA damage to mutation in bacteria may provide new avenues of
approach to human carcinogenesis, since at least some activities analogous
to components of the SOS response have been demonstrated in human cells.

## Key facts

- **NIH application ID:** 3124812
- **Project number:** 5R01AI010778-18
- **Recipient organization:** RUTGERS, THE STATE UNIV OF N.J.
- **SAM.gov UEI:** M1LVPE5GLSD9
- **Principal Investigator:** EVELYN M WITKIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $168,807
- **Award type:** 5
- **Project period:** 1975-01-01 → 1990-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124812

## Citation

> US National Institutes of Health, RePORTER application 3124812, REGULATION OF SOS FUNCTIONS IN ESCHERICHIA COLI (5R01AI010778-18). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124812. Licensed CC0.

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