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

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

Aubin J, Lemieux M, Tremblay M, Berard J, Jeannotte L.

Centre de recherche en cancerologie de l'Universite Laval, Centre Hospitalier
Universitaire de Quebec, 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.

PMID: 9441679 [PubMed - indexed for MEDLINE]


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