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Analysis of Cdh22 expression and function in the developing mouse brain.

Jonna Saarimäki-Vire¹, Annamari Alitalo, Juha Partanen

¹Department of Biosciences, University of Helsinki, Helsinki, Finland.

Developmental Dynamics : an Official Publication of the American Association of Anatomists

|July 16, 2011

Summary

This summary is machine-generated.

Cadherin-22 (Cdh22) is crucial for brain development, but its loss did not cause expected defects. Functional redundancy among type II cadherins likely compensates for Cdh22 loss in mouse brain development.

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Area of Science:

Developmental Biology
Neuroscience
Cell Adhesion

Background:

Classical cadherins are vital cell adhesion molecules for brain development.
Cadherin-22 (Cdh22), a type II cadherin, is expressed at the midbrain-hindbrain boundary.
Cdh22 is downregulated in Fgfr1 mutant mouse embryos with disrupted midbrain-hindbrain borders.

Purpose of the Study:

To investigate the expression patterns of Cdh22 and related type II cadherins in the developing mouse brain.
To determine the function of Cdh22 in brain development using a mutated allele.

Main Methods:

Detailed expression analysis of Cdh22, Cdh11, Cdh8, and Cdh6 in developing mouse brain.
Utilizing a Cdh22 mutated allele to study loss-of-function effects in mouse embryos.

Main Results:

Complementary and overlapping expression patterns were observed for Cdh22, Cdh11, Cdh8, and Cdh6 in the forebrain and midbrain.
Loss of Cdh22 led to reduced postnatal viability in mutant mice.
No significant defects in brain compartmentalization or nuclei formation were observed in Cdh22 mutants despite strong expression.

Conclusions:

Cdh22 plays a role in postnatal survival but is not essential for midbrain and forebrain compartmentalization.
Functional redundancy among type II cadherins may compensate for the loss of Cdh22 during brain development.