Abstract
To uncover roles for theHoxa-5gene during embryogenesis, we have focused on identifying structural and functional defects in organ systems underlying the perinatal lethality inHoxa-5homozygous mutants. Analysis of the mutant phenotype shows thatHoxa-5is 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 ofHoxa-5function results in alteredTTF-1, HNF-3β,and N-mycgene expression in the pulmonary epithelium. Since expression ofHoxa-5is 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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