# Role of POT1 in telomere length regulation

> **NIH NIH R01** · YALE UNIVERSITY · 2024 · $335,000

## Abstract

Project Summary
We will use state-of-the-art biochemical, cellular and genetic approaches to understand
mechanistically how ssDNA binding proteins protect telomeres from activating a DNA damage
response, regulate its length and replication. Using novel in vitro biochemical assays, we will
examine whether the molecular distinctions between RPA and hPOT1 underlie their unique
functions at telomeres. We will define the residues in hPOT1 that are required to repress telomere
end protection and C-strand resection (Aim 1). We will determine mechanistically how POT1b
promotes telomere length maintenance, and use hematopoietic stem cells conditionally depleted
of endogenous POT1a/b to define the amino acid residues involved in telomere elongation
necessary for the stem cell maintenance (Aim 2). We will explore how POT1a protects telomeres
from replication stress. Finally, we used BioID to identify Claspin as a telomere interacting protein
involved in DNA replication at telomeres devoid of POT1a (Aim 3). The proposed studies present
a unique opportunity to address some of the most important questions in the telomere field.

## Key facts

- **NIH application ID:** 10786055
- **Project number:** 5R01GM141350-03
- **Recipient organization:** YALE UNIVERSITY
- **Principal Investigator:** Sandy S Chang
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $335,000
- **Award type:** 5
- **Project period:** 2022-05-09 → 2025-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10786055

## Citation

> US National Institutes of Health, RePORTER application 10786055, Role of POT1 in telomere length regulation (5R01GM141350-03). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10786055. Licensed CC0.

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