# The role Akirin and Pannier interactions during myogenesis

> **NIH NIH R16** · KENNESAW STATE UNIVERSITY · 2024 · $135,500

## Abstract

Project Summary
Myogenic defects, which includes congenital heart malformations as well as congenital muscular dystrophies
are the most prevalent classes of birth defects in the human population, with an incident rate as high as 10 in
1000 live births. A significant number of these cases are termed sporadic, which are largely the result of
interactions between a number of independent genetic loci and alleles. To aid in our understanding of the
polygenic nature of congenital myogenic defects, it remains imperative to continue to identify new gene
regulatory partners that may play a role in the process of embryonic heart and skeletal muscle patterning. Our
laboratory has recently identified a cofactor, Akirin, that is responsible for interfacing transcription factor activity
with chromatin remodeling machinery to facilitate gene expression during a variety of skeletal myogenic and
cardiogenic processes. To date, the number of developmentally critical transcription factors known to interact
with Akirin remains frustratingly low, despite the myriad developmental processes known to require Akirin for
proper function. Excitingly, our preliminary data suggests that Akirin likely regulates insect embryonic heart
development and/or skeletal muscle development through interactions with the GATA-family member Pannier,
a zinc finger transcription factor identified as key for embryonic segmentation as well as cardiomyoblast
specification.
This project therefore involves simultaneous pursuit of two related specific aims: 1) Using a combination of
genetic, biochemical, and live imaging techniques, will confirm the importance of Akirin/Pannier interactions
during development, and 2) We will deploy a focused candidate screen for Akirin interacting loci, based on a
small number (25) of predicted Akirin interactors. This work will provide key data for understanding the role of
Akirin in the process of skeletal muscle and heart formation, and generate a further list of Akirin-interacting locian
Akirin interactome- that will shed light on other myogenic regulatory nodes that require Akirin.
Critically, in keeping with the goals of the Su RE award mechanism, this project will support the research
activities of the Pl, whose previously NIH-supported laboratory has an established track record of recruiting
talented undergraduate researchers from diverse backgrounds. Members of the Nowak Laboratory gain
hands-on experience in a wide variety of molecular, genetic, histological, microscopic, and biochemical
techniques, and are actively involved in not only project conception and execution, but also dissemination of
results and findings through conference presentations and authorships on peer-reviewed manuscripts.

## Key facts

- **NIH application ID:** 10815730
- **Project number:** 5R16GM145448-03
- **Recipient organization:** KENNESAW STATE UNIVERSITY
- **Principal Investigator:** Scott James Nowak
- **Activity code:** R16 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $135,500
- **Award type:** 5
- **Project period:** 2022-04-15 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10815730

## Citation

> US National Institutes of Health, RePORTER application 10815730, The role Akirin and Pannier interactions during myogenesis (5R16GM145448-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10815730. Licensed CC0.

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