# Evolution of gene regulatory networks controlling post-embryonic morphogenesis

> **NIH NIH F32** · NEW YORK UNIVERSITY · 2020 · $17,063

## Abstract

Evolution of gene regulatory networks controlling post-embryonic morphogenesis
Morphogenesis, or the development of form, is a universal process during development of multicellular
organisms that is controlled by the precise spatiotemporal expression of genes within gene regulatory networks
(GRNs). While advances have been made in elucidating GRNs that control embryonic development in model
organisms, we lack an understanding of how GRNs regulate post-embryonic morphogenesis and how these
networks evolve. The hotspot hypothesis predicts that the architecture of GRNs can bias evolution, such that
morphologies evolve via repeated co-option of a master regulator (i.e. a gene that is required and sufficient for
morphogenesis). This proposal will use a post-embryonic morphogenic process, known as Tail Tip
Morphogenesis (TTM), which evolved multiple times independently in Caenorhabditis elegans and related
species, to investigate the architecture and evolution of GRNs, and test the hotspot hypothesis. In C. elegans,
DMD-3, a DM-domain transcription factor, is the master regulator within the GRN governing TTM. Aim 1 uses
single-tissue RNA-Seq in a time series over the course of TTM in lineages where TTM independently evolved.
Then computationally infer the GRN underlying TTM in each species. The inferred GRNs will be used to test
the hotspot hypothesis and will contribute to our general understanding of how GRNs drive morphogenesis and
how plastic GRN architectures can be. Aim 2.1 validates the hotspot hypothesis by knocking out dmd-3, or
another candidate regulator inferred from Aim 1, in species where TTM independently evolved. Aim 2.2
validates the predicted downstream interactions within the GRN by using single-tissue RNA-Seq on the
regulator knockout lines. Aim 3 investigates the functional role of conserved modules (i.e. sets of genes and
their interactions) within the GRNs that have human homologs. As DMD-3 is a homolog to DMRT-1, required
for male fates in humans, regulators and effectors of DMD-3 could be candidate targets for future drugs or
therapies that could, for example, help people with sex reversal. Additionally, because morphogenesis is a
universal developmental process, this work will also likely identify genes that are conserved in other
morphogenic processes, such as cancer metastasis, regeneration, and wound healing.
This project will be conducted within the Center for Developmental Genetics at New York University, a world-
renowned research institution with top-notch resources and faculty, under the advisement of Prof. David Fitch
who has 25 years of experience as a researcher, mentor, and educator in the field of evolutionary
developmental biology. My training goals are to 1) expand my knowledge in developmental biology, 2) learn
developmental genetics wet lab techniques, 3) continue my education in bioinformatics, 4) develop teaching
and mentoring skills, 5) develop species related to C. elegans into satellite model systems to u...

## Key facts

- **NIH application ID:** 9911548
- **Project number:** 1F32GM136170-01
- **Recipient organization:** NEW YORK UNIVERSITY
- **Principal Investigator:** Alyssa Woronik
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $17,063
- **Award type:** 1
- **Project period:** 2020-06-01 → 2020-08-21

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9911548

## Citation

> US National Institutes of Health, RePORTER application 9911548, Evolution of gene regulatory networks controlling post-embryonic morphogenesis (1F32GM136170-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9911548. Licensed CC0.

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