# RADIATION-INDUCED CELL CYCLE DELAYS IN FISSION YEAST

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1993 · $173,960

## Abstract

When cells suffer DNA damage cellular feedback or "checkpoint" controls
delay entry to mitosis and the initiation of DNA synthesis.  We intend
to determine the mechanism by which gamma-radiation-induced DNA damage
results in such cell cycle delays in the fission yeast
(Schizosaccharomyces pombe).  The investigation will be in three parts.

l. Our observations indicate that radiation-induced mitotic delay is
imposed by inactivation of the mitotic kinase p34cdc2 We suggest that in
addition to changes in its state of phosphorylation, down-regulation of
p34 requires inactivation of cyclin (cdcl3+ product). This will be
investigated by monitoring and manipulating levels of cdc13 product and
message after irradiation.

2. Preliminary findings reveal an interaction between gene products which
are required for the imposition of mitotic delay by irradiation (radl7
product) and the tumor suppressor protein p53 (when the latter is
expressed in the fission yeast).  The literature indicates that p53 may
be required for the cell to delay DNA synthesis in response to
irradiation.  We will therefore a) determine whether radl7-W (and similar
checkpoint mutants) fail to delay DNA synthesis initiation after
irradiation and, b) characterize other gene products, identified by
genetic procedures, which interact with the tumor suppressor protein.
This approach may allow elucidation of both the mechanism of DNA
synthesis delay and the function of p53.

3. To date no attempt has been made to identify conditional checkpoint
mutants. Therefore, mutations in checkpoint control elements which are
essential for viability are under-represented in known mutant series.
Temperature-sensitive checkpoint mutants will be sought.  Mutants will
allow further genetic and molecular genetic characterization of the DNA
damage checkpoint control.

Use of the fission yeast, which has been extensively characterized for
G2 cell cycle controls and checkpoint controls, allows a molecular
genetic approach to this investigation.  These studies will contribute
to an understanding of cell cycle controls and their involvement in
radiation responses and, conceivably, oncogenesis.

## Key facts

- **NIH application ID:** 3179937
- **Project number:** 2R01CA040245-07A2
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** ROY ROWLEY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $173,960
- **Award type:** 2
- **Project period:** 1985-01-15 → 1996-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3179937

## Citation

> US National Institutes of Health, RePORTER application 3179937, RADIATION-INDUCED CELL CYCLE DELAYS IN FISSION YEAST (2R01CA040245-07A2). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3179937. Licensed CC0.

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