Analysis of Cdh22 expression and function in the developing mouse brain

Classical cadherins are important cell adhesion molecules specifying and separating brain nuclei and developmental compartments. Cadherin‐22 (Cdh22) belongs to type II subfamily of classical cadherins, and is expressed at the midbrain‐hindbrain boundary during early embryogenesis. In Fgfr1 mutant mo...

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Bibliographic Details
Published in:Developmental dynamics 2011-08, Vol.240 (8), p.1989-2001
Main Authors: Saarimäki‐Vire, Jonna, Alitalo, Annamari, Partanen, Juha
Format: Article
Language:English
Subjects:
Animals
Brain - anatomy & histology
Brain - embryology
Brain - metabolism
Cadherins - genetics
Cadherins - metabolism
Cdh11
Cdh22
Cdh6
Cdh8
cell adhesion
compartment boundary
diencephalon
Embryo, Mammalian - anatomy & histology
Embryo, Mammalian - physiology
Extremities - anatomy & histology
Extremities - embryology
FGF signaling
forebrain
Gene Expression Regulation, Developmental
Genotype
hindbrain
isthmic organizer
Male
Mice
midbrain
Morphogenesis - physiology
Mutation
neurogenesis
Survival Rate
Testis - anatomy & histology
Testis - embryology
Testis - metabolism
type II cadherin
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Summary:Classical cadherins are important cell adhesion molecules specifying and separating brain nuclei and developmental compartments. Cadherin‐22 (Cdh22) belongs to type II subfamily of classical cadherins, and is expressed at the midbrain‐hindbrain boundary during early embryogenesis. In Fgfr1 mutant mouse embryos, which have a disturbed midbrain‐hindbrain border, Cdh22 is down‐regulated. Here, we studied expression of Cdh22 in developing mouse brain in more detail and compared it to expression of related family members. This revealed both complementary and overlapping patterns of Cdh22, Cdh11, Cdh8, and Cdh6 expression in distinct regions of the forebrain and midbrain. We used a mutated allele of Cdh22 to study its function in brain development. Loss of Cdh22 caused reduced postnatal viability. Despite strong Cdh22 expression in the developing brain, we did not observe defects in compartmentalization or abnormalities in the midbrain and forebrain nuclei in Cdh22 mutants. This may be explained by functional redundancy between type II cadherins. Developmental Dynamics 240:1989–2001, 2011. © 2011 Wiley‐Liss, Inc.
ISSN:1058-8388
1097-0177
DOI:10.1002/dvdy.22686