# Actin cytoskeleton from nucleus to organism

> **NIH NIH R35** · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · 2020 · $382,036

## Abstract

PROJECT SUMMARY/ABSTRACT
 Textbooks teach us that actin filaments give cells their shape, and that a “parts list” of proteins drives
actin remodeling when cells change shape. But what is missing from this simple telling is a holistic understanding
of how upstream gene expression and signaling control actin remodeling, how different proteins work together
to remodel actin, and how downstream cell shape change is converted into timely and reliable organismal out-
comes. Because actin-based failures can stem from events before, during and after remodeling, we need an
integrated understanding to make sense of actin’s critical role in health and disease.
 To obtain this kind of “whole picture” view of actin, my lab studies cellularization, the first tissue-building
event in Drosophila embryos. We developed this simple experimental system so that we can study the actin
remodeling that drives cellularization, while also relating that remodeling to upstream events at the level of gene
expression and signaling, and downstream outcomes including morphogenetic fidelity and embryonic viability.
Our methods combine Drosophila genetics and embryology with quantitative live-cell imaging of mRNAs, actin,
and actin regulatory proteins, down to single-molecule resolution.
 Our long-term objective is to understand how the actin cytoskeleton interacts with subcellular processes
(e.g. transcription) and systems (e.g. nucleus) to orchestrate cell shape change with “the right” kinetics, robust-
ness and mechanical properties to achieve successful organismal outcomes. In the next five years, we will focus
on three goals arising from our ongoing studies: Goal 1. Determine how gene expression regulates actin remod-
eling – Gene expression instructs morphogenesis. Yet, we do not know how transcriptional dynamics inform
actin remodeling. For cellularization, five genes that encode actin regulators must be transcribed. We will test a
hypothesis that quantitative features of transcription of these genes underpin the global synchrony and uniformity
of cellularization in embryos. Goal 2. Determine mechanisms of actomyosin contraction – Actomyosin contraction
is essential to cell shape change, but its mechanism is controversial. During cellularization, actomyosin rings
contract in back-to-back phases that are mechanistically distinct (Myosin-2 dependent versus independent). We
will determine how actin binding proteins drive each mechanism. Goal 3. Determine how the actin cytoskeleton
responds to environmental stress – Actin is increasingly recognized as a mediator of stress response. We re-
cently identified a heat inducible Actin Stress Response (ASR) in embryos. We will test the hypothesis that ASR
puts embryo viability at risk by altering homeostasis between free actin pools in the cytoplasm and nucleus.
 These goals build on each other so that we will understand how mechanisms before, during and after
actin remodeling work together to determine outcomes for the embryo. Our e...

## Key facts

- **NIH application ID:** 9931996
- **Project number:** 1R35GM136384-01
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN
- **Principal Investigator:** Anna Sokac
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $382,036
- **Award type:** 1
- **Project period:** 2020-08-15 → 2025-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9931996

## Citation

> US National Institutes of Health, RePORTER application 9931996, Actin cytoskeleton from nucleus to organism (1R35GM136384-01). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/9931996. Licensed CC0.

---

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