Flagship Project

DNMT3A mechanotransduction during cutaneous wound repair

This is the project I return to most often when I try to describe my current research. I wanted to understand how the physical changes created by a wound are read inside the nucleus during epidermal repair, and DNMT3A became the entry point into that question.

First-author project Mechanobiology and epigenetics Epidermal repair

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Overview

Why this project matters

I was drawn to this problem because a wound is not only a biochemical event. It changes tension, shape, cytoskeletal organization, and the physical conditions that epidermal cells experience in real time. What interested me was how those changes become something a cell can carry into the nucleus and act on.

DNMT3A became important to me because it offered a way to connect mechanics to epigenetic decision-making. The project follows how wound-associated mechanics regulate its nucleocytoplasmic partitioning, and why that movement may matter for repair-associated cell-state change.

Core Questions

The questions that shaped the work

What changes at the wound edge?

I started from the idea that injury changes the local physical state of tissue in ways that do more than accompany repair. They may actually help instruct it.

How is a nuclear regulator repositioned?

A central question for me was how actin remodeling and ERK1/2 signaling participate in moving DNMT3A during the repair response, and whether that movement is part of the logic of healing.

Why does localization matter?

What kept the project interesting was the possibility that mechanotransduction is not just upstream signaling, but part of how epigenetic decisions are organized during state change.

Approach

Experimental frame

I approached the project by trying to keep mechanics, signaling, and nuclear behavior in the same frame. That meant combining molecular biology, biochemistry, fluorescence microscopy, and mechanobiology-oriented analysis rather than treating them as separate layers.

The important thing for me was not simply whether DNMT3A moves. It was whether cytoskeletal perturbation, signaling behavior, and nuclear relocalization could be interpreted together as part of a wound-state logic rather than as disconnected observations.

Associated Outputs

Where this work appears

Primary output

2026 bioRxiv first-author preprint

Actin-dependent mechanotransduction controls nucleocytoplasmic partitioning of DNMT3A through ERK1/2 signaling during cutaneous wound healing.

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Broader context

Mechanics, chromatin, and repair

This is where the broader shape of my research program becomes most visible to me: physical cues at wounds feeding into nuclear regulation and regenerative state change.

Why it is central

A narrative anchor for the academic profile

If someone asks what sits at the mechanistic center of my current research identity, this is usually the project I would start with.

Other projects in the portfolio

Contact

Interested in this direction of work?

I would be especially glad to talk with people interested in mechanobiology, chromatin regulation, regenerative systems, and postdoctoral directions that connect these areas.

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