# INDUCIBLE RESPONSES TO CARCINOGENIC DNA DAMAGE

> **NIH NIH R01** · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · 1988 · $159,320

## Abstract

Our broad objective is to understand inducible cellular responses to DNA
damage by carcinogens, many of which are mutagens in bacteria, with special
emphasis on understanding the relationship between those responses that
contribute to cellular survival following carcinogenic damage and those
which affect mutagenesis.  We use Escherichia coli as a model cell system
in which to study inducible SOS responses and adaptive responses, evidence
for both of which has also been found in mammalian cells, because of the
advantage of availability of relevant mutants and extensive biochemical and
genetic characterization.  Immediate research objectives include:  (1) Gene
products involved in inducible repair of UV damage.  Having evidence that
long patch repair synthesis may be the primary SOS process effecting
enhanced cellular survival, we are attempting to identify the gene products
that participate in this process.  In particular, the possible involvement
of an altered polymerase will be tested and the nature of the requirement
for the recA gene will be examined.  Whether long patch synthesis proceeds
by a mechanism involving the recF pathway will be investigated.  (2)
Substrate for long patch repair of UV damage.  Having evidence suggesting
that long patches occur at a small class of damage sites that are
refractory to constitutive repair and that are potent blocks to
replication, we are investigating the nature of these sites as an approach
to understanding the means by which the inducible process contributes to
survival.  We are particularly interested in the possibility that lesions
in some functionally distinct regions of the genome, perhaps growing point
regions or actively transcribing genes, are involved.  (3) Repair of
alkylation damage.  Having evidence that SOS induction promotes survival of
alkylation damage in addition to UV damage, we are attempting to determine
the interaction of the SOS and adaptive responses in excision repair and
mutagenesis after treatment with alkylating agents.  Effects of the two
inducible processes on repair synthesis and on adduct removal will be
compared.  The possibility that glycosylase action significantly precedes
AP endonuclease action in repair of alkylation damage, thereby generating
important premutagenic lesions (AP sites) as a consequence of repair, will
be examined.

## Key facts

- **NIH application ID:** 3170895
- **Project number:** 5R01CA032986-06
- **Recipient organization:** UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB
- **SAM.gov UEI:** ENBLDJUN4N73
- **Principal Investigator:** Priscilla K. Cooper
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $159,320
- **Award type:** 5
- **Project period:** 1982-09-01 → 1990-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3170895

## Citation

> US National Institutes of Health, RePORTER application 3170895, INDUCIBLE RESPONSES TO CARCINOGENIC DNA DAMAGE (5R01CA032986-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3170895. Licensed CC0.

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