A maternally established gradient of nuclear Dorsal protein is the first step in subdivision of the Drosophila neurectoderm into stripes of homeodomain gene expression. Dorsal in combination with the EGF and TGFbeta signaling pathways are key regulators of the expression of the genes ventral nervous system defective (vnd), intermediate neuroblasts defective (ind), and muscle segment homeobox (msh) in the developing neurectoderm. These three genes encode homeodomain transcription factors that can repress each other, which ensures adjacent, non-overlapping expression domains. Expression of vnd, ind, and msh is maintained after decline in EGF and TGFbeta signaling, but the relevant positive transcriptional regulators have not yet been defined. Here, we show that Ind can bind DNA with the same sequence specificity as its murine ortholog Gsh1. We have identified a novel upstream regulatory element at the ind locus containing predicted Ind binding sites, and we show that Ind activity is both necessary and sufficient for reporter gene expression from this element. We conclude that Ind can act as a transcriptional activator, and that positive autoregulation of Ind is a mechanism for persistent ind expression within the developing embryonic nervous system.
Initiation and refinement of expression of the Ind homeodomain protein in the Drosophila embryo is coordinately regulated by global dorsoventral patterning pathways Dorsal, Egfr, and Dpp, and well as by Vnd, which positions the ventral boundary of Ind. Therefore, we set out to look for novel regulators of dorsoventral patterning by screening the Exelixis deficiency collection for modified expression of Ind. Indeed, we found deficiencies that remove components of the known signaling pathways had altered or lost ind expression. These findings included deficiencies that remove screw, dpp, and egfr as well as deficiencies that remove ind itself. In addition, we found several deficiencies that had altered or loss of ind expression. We also observed phenotypes suggestive of dorsoventral patterning defects such as twisting during gastrulation, and defects associated with loss of dorsal specification. These include a pair of overlapping deficiencies that produced ventralized embryos. We find that transheterozygotes of these two deficiencies are also ventralized. There are seven genes common to both deficiencies, including CG11582, which encodes a twisted gastrulation-like protein. These two deficiencies are also allelic with shrew mutations. Here, we present data supporting the conclusion that CG11582 is the gene affected in shrew mutants. Developmental Dynamics 236:3524 -3531, 2007.
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