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Dev Biol. 1997 Dec 15;192(2):432-45.

Early postnatal lethality in Hoxa-5 mutant mice is attributable to respiratory tract defects.

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  • 1Centre de recherche en cancérologie de l'Université Laval, Centre Hospitalier Universitaire de Québec, Canada.


To uncover roles for the Hoxa-5 gene during embryogenesis, we have focused on identifying structural and functional defects in organ systems underlying the perinatal lethality in Hoxa-5 homozygous mutants. Analysis of the mutant phenotype shows that Hoxa-5 is essential for normal organogenesis and function of the respiratory tract. In homozygous newborn mutants, improper tracheal and lung morphogenesis can lead to tracheal occlusion, and to respiratory distress associated with a marked decrease in the production of surfactant proteins. Collectively, these defects likely underlie the pronounced mortality of homozygous mutant pups. Furthermore, the loss of Hoxa-5 function results in altered TTF-1, HNF-3 beta, and N-myc gene expression in the pulmonary epithelium. Since expression of Hoxa-5 is confined to the mesenchymal component of the developing trachea and lung, the effects observed in epithelial cells may result from a disruption of normal epithelial-mesenchymal interactions.

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