# Understanding transient dynamics in genomic state regulation during regeneration

> **NIH NIH F31** · UNIVERSITY OF WASHINGTON · 2020 · $38,140

## Abstract

ABSTRACT
Humans have almost no regenerative capability following limb loss, resulting in decreased
quality of life. In contrast, amphibians have the capability to scarlessly regenerate appendages.
Following injury, complex genetic processes need to be initiated with high spatial and temporal
resolution. Xenopus tropicalis are diploid frogs, whose tadpoles scarlessly regenerate properly
patterned tails after amputation in approximately 72 hours, making them an ideal system to
query genomic changes that occur during regeneration. An Assay for Transposase Accessible
Chromatin (ATAC-seq) in Xenopus has shown that at 6 hours post amputation (hpa)
differentially accessible regions of chromatin are inaccessible, and then at 24 hpa specific
regions of chromatin regain accessibility. This leads to the question: how are transient changes
in chromatin accessibility achieved? Studies on transient changes in gene expression during
development across species have elucidated two factors of regulation: changes in epigenetic
state, and nuclear lamina association. EZH2 methylates H3K27 and has a critical role in
development. EZH2 has also been shown to be required for regeneration in a variety of model
systems including Xenopus. H3K27Me3 is an epigenetic mark that can correspond to facultative
heterochromatin, and when found in conjunction with H3K4Me3 can be a mark of “poised”
regions of chromatin, however, H3K4Me3 alone is a mark of active promoters. By studying the
dynamics of methylation state and lamina association, I will gain insight into the dynamics of
several different chromatin states over the course of regeneration and how these changes alter
chromatin accessibility. Aim 1 will focus on the spatiotemporal dynamics of transient changes in
epigenetic state, by determining the distribution of H3K27Me3, H3K4Me3, and regions of
chromatin that interact with the nuclear lamina. I will identify if regions of developmental
enhancers and promoters that are transiently inactivated during the early stages of
regeneration. In Aim 2 I will query how changes in methylation state alter chromatin accessibility
and gene expression during regeneration. This study will utilize cutting edge assays such as
CUT&RUN and ATAC-seq together with functional analyses to probe the mechanism of
transient changes in genomic programming during regeneration and how this may parallel
developmental processes.

## Key facts

- **NIH application ID:** 10008966
- **Project number:** 5F31HD097910-02
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** Hannah Arbach
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $38,140
- **Award type:** 5
- **Project period:** 2019-09-16 → 2021-06-11

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10008966

## Citation

> US National Institutes of Health, RePORTER application 10008966, Understanding transient dynamics in genomic state regulation during regeneration (5F31HD097910-02). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10008966. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*