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Protein Modification and Stability Regulation to Cope with Genotoxic Environments

Award Number: F31ES036884
ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 02/01/2025
PERIOD OF PERFORMANCE END DATE: 01/31/2028

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Protein Modification and Stability Regulation to Cope with Genotoxic Environments - PROJECT SUMMARY/ABSTRACT Humans face many types of environmental genotoxic agents, such as various pollutants and radiation, that can cause deleterious mutations and diseases. To survive and adapt to genotoxic conditions, cells rely on many highly conserved and complex molecular strategies. One strategy to withstand genotoxic stress is the use of error-prone repair mechanisms to increase mutation rates, which can potentiate new functions for better adaptation to toxic environments. Another mechanism is the DNA damage checkpoint (DDC) system, which controls the arrest and resumption of the cell cycle in accordance with the burden of genomic lesions. While the frameworks of both strategies are largely established, important mechanistic details are lacking. To address these gaps in knowledge, I will capitalize on the budding yeast model organism’s highly conserved DDC and repair systems. Aim 1 will build on the recent observation that the desumoylase Ulp1 is sumoylated upon genotoxin treatment and that mutating its two sumoylation sites results in a phenotype indicative of increased homologous recombination (HR). I thus hypothesize that Ulp1 sumoylation suppresses HR to favor error-prone repair. I will test this hypothesis and define the broader SUMO-based control of DNA repair pathway usage in response to genotoxins. Aim 2 will address the recent findings that RPA is downregulated after genotoxin exposure. I hypothesize that RPA downregulation can induce DDC recovery. To test this, I will elucidate how RPA degradation is regulated and how this impacts DDC recovery. Defects in either of the DNA repair pathway choices and DDC responses can lead to genome instability syndromes, characterized by increased sensitivity to environmental genotoxins, developmental abnormalities, and increased tumorigenesis. This work will lay the foundation for elucidating cellular adaptation strategies and can inform disease prevention and treatment strategies. It will also provide important training for me to reach my long-term career goal of becoming a principle investigator studying how human cells response to environmental genotoxins.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $48,974 )
2026	2026	WEILL MEDICAL COLLEGE OF CORNELL UNIVERSITY	575 LEXINGTON AVE FL 9	NEW YORK	NY	10022	NEW YORK	USA	Environmental Health	000	2	1/21/2026	NON-COMPETING CONTINUATION	$48,974
														Subtotal = $48,974

Issue Date FY: 2024 ( Subtotal = $48,974 )
2024	2024	WEILL MEDICAL COLLEGE OF CORNELL UNIVERSITY	575 LEXINGTON AVE FL 9	NEW YORK	NY	10022	NEW YORK	USA	Environmental Health	000	1	8/5/2024	NEW	$48,974
														Subtotal = $48,974

Grand Total All Awards = $97,948

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Protein Modification and Stability Regulation to Cope with Genotoxic Environments

Award Number: F31ES036884

ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 02/01/2025

PERIOD OF PERFORMANCE END DATE: 01/31/2028

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