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Related Experiment Video

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Using Confocal Analysis of Xenopus laevis to Investigate Modulators of Wnt and Shh Morphogen Gradients

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Forces shaping a Hox morphogenetic gene network.

Sol Sotillos¹, Mario Aguilar, James Castelli-Gair Hombría

¹Centro Andaluz de Biología del Desarrollo, Consejo Superior de Investigaciones Científicas, Junta de Andalucía, Universidad Pablo de Olavide, 41013 Seville, Spain.

Proceedings of the National Academy of Sciences of the United States of America

|February 27, 2013

Summary

This summary is machine-generated.

The Abdominal-B protein coordinates gene networks for organ development. Its effector, Crossveinless-c (Cv-c), initially destabilizes cells, but compensatory mechanisms evolve, explaining complex gene network formation.

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

The Abdominal-B selector protein orchestrates posterior spiracle organogenesis through a complex gene network.
The evolutionary origins and selective pressures shaping such intricate networks remain largely unknown.
Understanding how these networks assemble, likely sequentially, is crucial for developmental biology.

Purpose of the Study:

To investigate the evolutionary origins of complex organogenetic gene networks.
To determine the morphogenetic effects of individual gene network effectors.
To elucidate the compensatory mechanisms that arise in response to novel regulator cooption.

Main Methods:

Expressing individual effectors of the Abdominal-B gene network in naive epithelial cells.
Analyzing the morphogenetic and cellular effects of Crossveinless-c (Cv-c) Rho GTPase-activating protein.
Examining compensatory mechanisms in spiracle cells and other epithelial cells co-opting Cv-c.

Main Results:

Most individual effectors have minimal morphogenetic impact, except for Cv-c.
Cv-c expression induces cell motility and down-regulates epithelial polarity and adhesion proteins.
Endogenously expressing cells, like spiracle cells, develop compensatory mechanisms against Cv-c's effects, involving guanine nucleotide exchange factor (GEF) proteins.

Conclusions:

Co-opting a novel morphogenetic regulator like Cv-c into a selector cascade initially causes cellular instability.
This instability creates selective pressure for the recruitment of compensatory molecules within the same cascade.
This provides an experimental basis for understanding the assembly of complex organogenetic gene networks.