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.

The Drosophila neurectoderm is initially subdivided across the dorsoventral (DV) axis into three domains that are defined by the expression of three homeodomain containing proteins. These are from ventral to dorsal: Ventral nervous system defective (vnd), Intermediate neuroblasts defective (ind) and Muscle segment homeobox (msh). This is remarkably similar to the distribution of the orthologous homeodomain proteins in the developing neural tube of mice and Zebrafish. This pattern is partially governed by a 'ventral dominance' mechanism, in which Vnd represses ind and Ind represses msh. A major unanswered question in this process is: How does Ind direct positioning of the ventral border of msh expression. Toward this goal, we have identified regulatory DNA essential for expression of msh in the early neurectoderm. In addition, we demonstrated that Ind acts directly in this element by a combination of genetic and molecular experiments. Specifically, expression is expanded ventrally in ind mutant embryos and Ind protein directly and specifically bound to the msh regulatory DNA, and this interaction was required to limit the ventral boundary of msh expression. Developmental