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We also have studied formation of the Sog protein gradient in the dorsal epidermal region of the embryo which we visualized [4] and analyzed quantitatively in collaboration with Arthur Lander’s group (UCI) [5].This BMP activity gradient arises as a consequence of an adjacent source/sink configuration wherein ventrally produced Sog diffuses dorsally, where it is degraded by the metalloprotease Tolloid and removed by endocytosis [4].Although formation of each vein is initiated separately, these linear structures are all induced by the same general mechanism (termed “for-export-only signaling”) in which cells in one domain produce a diffusible factor to which they are unable to respond [10].The vein inducing signal diffuses into the adjacent cell territory where cells nearest the source of the signal can respond by activating expression of vein specific identity genes such as as a candidate gene involved in Angelman syndrome [15], to examine an interaction between g-secretase and peroxiredoxins that may be relevant to Alzheimer’s disease [16], to identify a cooperative interaction between the cell adhesion molecule DSCAM and a collagen subunit (COL6A2) that when over-expressed leads to congenital heart defects in flies and mice and may contribute to heart defects in Down syndrome patients (in collaboration with Geoff Rosenfeld, UCSD, Medicine) [17], and, in collaboration with Michael Karin (UCSD, Pharmacology) to examine mechanisms of metabolic homeostasis relevant to aging [18].

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For example, most recently, we have proposed that differences in gene length alone can create a transient nested pattern of gene expression to help “seed” morphogen-dependent patterning across a developing field of cells [24].

We have also developed bioinformatic tools for mining and comparing genome data [25, 26].

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