# GENETIC CONTROL OF EMBRYOGENESIS IN C ELEGANS

> **NIH NIH R01** · UNIVERSITY OF COLORADO · 1994 · $141,968

## Abstract

The long term objective of this project is to elucidate mechanisms of
determination in animal embryonic development, using the nematode
Caenorhabditis elegans as an experimental system.  In the C elegans
embryo, determination of cell fates is a hierarchical process: the
primary determinants are probably localized, maternally derived
macromolecules, whose effects are secondarily modified by establishment
of sexual identity and by cell interactions controlling expression of
embryonic genes that further dictate cell-type determination.  This
project will continue to investigate the mechanisms of sex determination
and the roles of embryonically expressed genes in patterning and cell
fate decisions.

In the first area, recent work from our laboratory has shown that her-1,
the initial major switch gene in the regulatory pathway that controls sex
determination, encodes a small secreted polypeptide that exerts its
masculinizing effects via transmembrane signalling.  To further elucidate
her-1 function, the regulation of its male-specific transcription will be
investigated, the active form of the her-1 product will be isolated and
its primary structure determined, and experiments will be undertaken to
identify its receptor by binding assays with embryonic cells in culture.
These studies could have eventual health implications for control of
human parasitic nematode infections.  In a related project, a small
region of the X chromosome that appears to be a component of the primary
signal for sex determination will be molecularly characterized.

In the area of cell-type determination, ongoing large-scale screens using
trimethyl-psoralen as a mutagen will be continued, with the goal of
saturation for non-maternal-effect mutations that result in specific
effects on embryonic patterning.  In the course of these screens, several
loci (nob genes) have been identified that mutate to cause similar severe
posterior patterning defects, and one of these has been shown to be a
previously identified homeobox gene (pal-1), homologous to the caudal
gene in Drosophila.  The remaining nob genes will be cloned for molecular
characterization, and their interactions with each other and with other
known embryonically expressed and maternal-effect genes will be
investigated by genetic as well as molecular methods, in an effort to
understand the control of posterior patterning in the embryo.  In light
of accumulating evidence that all animal embryos employ similar
determination mechanisms, these studies are likely to contribute
eventually to understanding of human hereditary birth defects and other
developmental disorders.

## Key facts

- **NIH application ID:** 2196840
- **Project number:** 5R01HD011762-17
- **Recipient organization:** UNIVERSITY OF COLORADO
- **SAM.gov UEI:** SPVKK1RC2MZ3
- **Principal Investigator:** WILLIAM B WOOD
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $141,968
- **Award type:** 5
- **Project period:** 1978-04-01 → 1998-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2196840

## Citation

> US National Institutes of Health, RePORTER application 2196840, GENETIC CONTROL OF EMBRYOGENESIS IN C ELEGANS (5R01HD011762-17). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2196840. Licensed CC0.

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