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Updated: Mar 21, 2026

Dissection of the Auditory Bulla in Postnatal Mice: Isolation of the Middle Ear Bones and Histological Analysis

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Published on: January 4, 2017

Temporal and spatial requirements for Hoxa3 in mouse embryonic development.

Jena L Chojnowski¹, Heidi A Trau¹, Kyoko Masuda¹

¹Department of Genetics, Paul D. Coverdell Center, University of Georgia, 500 DW Brooks Drive, Athens, GA, 30602, USA.

Developmental Biology

|May 15, 2016

Summary

HOXA3 is crucial for pharyngeal organ development, acting both within cells and on surrounding tissues. It guides tissue organization, differentiation, migration, and morphogenesis in various cell types.

Keywords:

HOXA3 Organogenesis Pharyngeal arches Temporal regulation Thymus Thyroid

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

Hoxa3(null) mice exhibit severe pharyngeal organ defects, including athymia and thyroid hypoplasia.
Altered structures in Hoxa3 mutants extend anterior to the gene's known expression boundary.
Understanding HOXA3's cellular targets and temporal requirements is essential for elucidating pharyngeal development.

Purpose of the Study:

To comprehensively analyze the temporal and tissue-specific requirements of Hoxa3.
To identify specific cellular targets of HOXA3 function during pharyngeal organ development.
To investigate HOXA3's role in both cell-autonomous and non-cell-autonomous processes.

Main Methods:

Utilized Hoxa3(null) mouse models.
Performed lineage analysis using Hoxa3(Cre) reporter mice.
Conducted a comprehensive temporal and tissue-specific analysis of Hoxa3 function.

Main Results:

HOXA3 functions cell-autonomously and non-cell-autonomously in 3rd and 4th arch derivatives.
HOXA3 acts in a neural crest cell (NCC)-specific, non-cell-autonomous manner for Hoxa3-negative structures.
HOXA3 is essential for tissue organization and differentiation in endodermal cells and for NCC migration and morphogenesis.

Conclusions:

HOXA3 plays diverse roles in pharyngeal organ development, including tissue organization, differentiation, migration, and morphogenesis.
Defects in Hoxa3 mutants are not due to altered positional identity but rather to HOXA3's control of distinct genetic programs.
This study provides a detailed map of HOXA3's action during the development of multiple pharyngeal structures.