Ventral abdominal wall dysmorphogenesis of Msx1/Msx2 double‐mutant mice

Abstract

Msx1 and Msx2 genes encode the homeodomain transcription factors. Several gene knockout mice and expression studies suggest that they possess functionally redundant roles in embryogenesis. In this study, we revealed that Msx1 and Msx2 were expressed during ventral body wall formation in an overlapping manner. Msx1/Msx2 double-mutant mice displayed embryonic abdominal wall defects with disorganized muscle layers and connective tissues. These findings indicate that Msx1 and Msx2 play roles in concert during embryonic ventral abdominal wall formation.

Molecular genetic cascades for external genitalia formation: An emerging organogenesis program

“…It has thus been speculated that GT development requires correct adjacent tissue differentiation, such as lower body wall formation. Abnormal lower body wall formation associated with bladder/cloaca extrophy often simultaneously displays genital abnormalities such as the upper GT defects, and epispadias (Zhang et al, 1996;Brewer and Williams, 2004;Ogi et al, 2005;Haraguchi et al, unpublished results). In relation with such phenotypes, the presence or absence of cell migration between the umbilical region (later the lower body wall) and the (upper) GT bud requires further analyses.…”

A new serine/threonine protein kinase,Omphk1, essential to ventral body wall formation

“…AP-2␣ (Brewer and Williams, 2004a), Hoxb2/b4 double (Manley et al, 2001), Tgf␤2/␤3 double (Dunker and Krieglstein, 2002), and Mab21l2 (Yamada et al, 2004) mutants have defects in the primary body wall formation. The AP-2␣ mutant also lacks sternal and abdominal bands (Brewer and Williams, 2004a), and several mutants are known that have defects in the migration of the bands and/or in the subsequent clo-sure of the ventral body wall (Suzuki et al, 1996;Eggenschwiler et al, 1997;Zhang et al, 1997;Kitamura et al, 1999;Carter et al, 2000;Rauch et al, 2000;Doyonnas et al, 2001;Ogi et al, 2005;Thumkeo et al, 2005). However, the number of genes that participate in the ventral body wall formation is still too limited to discuss the molecular events of formation of this wall or pathologies of human defects.…”

Generation of an Msx2‐GFP conditional null allele

“…Moreover, even at early stages, the complexity of the phenotype, the numerous embryological fields affected, and the interference between the defects elicited by the double mutation render the analysis difficult. For example, double mutants suffer from thoracoabdominoschisis (opening of both thorax and abdomen) (Ogi et al, 2005), which alters the development of all internal organs, and thus precludes the analysis of the role of Msx genes in these organs.…”