Molecular analysis of even-skipped mutants in Drosophila development.

Abstract

The homeo box gene even-skipped (eve) plays a key role in the regulation of the Drosophila segmentation pattern. eve- embryos lack segment borders and show altered activities of several segmentation genes, including fushi tarazu (ftz), engrailed (en), and wingless (wg). Here, we present evidence that eve influences its own expression in a tissue-specific manner. Each of four different eve mutations disrupts the normal eve expression pattern, and null mutations cause a premature loss of eve products in ectodermal, but not mesodermal, tissues. Molecular characterization of eve mutations indicates that disruptions of the eve pattern are not due to alterations in the eve promoter but, instead, involve abnormal eve proteins. Two different eve mutations cause single amino acid substitutions within the homeo box, and we discuss the implications of these changes with regard to homeo box gene function. We also present evidence that eve+ gene activity is not only required for the activation of the odd-numbered en stripes but also for the correct positioning of each ftz stripe. We present a model for the loss of en expression in eve- embryos, based on the concentration-dependent regulation of the ftz pattern by eve+ products.