Changes in gene expression during animal development are largely responsible for the evolution of morphological diversity. However, the genetic and molecular mechanisms responsible for the origins of new gene-expression domains have been difficult to elucidate. Here, we sought to identify molecular events underlying the origins of three novel features of wingless (wg) gene expression that are associated with distinct pigmentation patterns in Drosophila guttifera. We compared the activity of cis-regulatory sequences (enhancers) across the wg locus in D. guttifera and Drosophila melanogaster and found strong functional conservation among the enhancers that control similar patterns of wg expression in larval imaginal discs that are essential for appendage development. For pupal tissues, however, we found three novel wg enhancer activities in D. guttifera associated with novel domains of wg expression, including two enhancers located surprisingly far away in an intron of the distant Wnt10 gene. Detailed analysis of one enhancer (the vein-tip enhancer) revealed that it overlapped with a region controlling wg expression in wing crossveins (crossvein enhancer) in D. guttifera and other species. Our results indicate that one novel domain of wg expression in D. guttifera wings evolved by co-opting pre-existing regulatory sequences governing gene activity in the developing wing. We suggest that the modification of existing enhancers is a common path to the evolution of new gene-expression domains and enhancers.enhancers | novelty | gene regulation | development | pigmentation

Vulval differentiation in Caenorhabditis elegans is controlled by a conserved signal transduction pathway mediated by Ras and a kinase cascade that includes Raf, Mek and MAPK. Activation of this cascade is positively regulated by a number of proteins such as KSR (kinase suppressor of Ras), SUR‐8/SOC‐2, SUR‐6/PP2A‐B and CDF‐1. We describe the functional characterization of sur‐7 and several genes that regulate signaling downstream of ras. We identified sur‐7 by isolating a mutation that suppresses an activated ras allele, and showed that SUR‐7 is a divergent member of the cation diffusion facilitator family of heavy metal ion transporters that is probably localized to the endoplosmic recticulum membrane and regulates cellular Zn2+ concentrations. Genetic double mutant analyses suggest that the SUR‐7‐mediated effect is not a general toxic response. Instead, Zn2+ ions target a specific step of the pathway, probably regulation of the scaffolding protein KSR. Biochemical analysis in mammalian cells indicates that high Zn2+ concentration causes a dramatic increase of KSR phosphorylation. Genetic analysis also indicates that PP2A phosphatase and PAR‐1 kinase act downstream of Raf to positively and negatively regulate KSR activity, respectively.

Sexual dimorphism is widespread throughout the metazoa and plays important roles in mate recognition and preference, sexbased niche partitioning, and sex-specific coadaptation. One notable example of sex-specific differences in insect body morphology is presented by the higher diptera, such as Drosophila, in which males develop fewer abdominal segments than females. Because diversity in segment number is a distinguishing feature of major arthropod clades, it is of fundamental interest to understand how different numbers of segments can be generated within the same species. Here we show that sex-specific and segment-specific regulation of the Wingless (Wg) morphogen underlies the development of sexually dimorphic adult segment number in Drosophila. Wg expression is repressed in the developing terminal male abdominal segment by the combination of the Hox protein Abdominal-B (Abd-B) and the sex-determination regulator Doublesex (Dsx). The subsequent loss of the terminal male abdominal segment during pupation occurs through a combination of developmental processes including segment compartmental transformation, apoptosis, and suppression of cell proliferation. Furthermore, we show that ectopic expression of Wg is sufficient to rescue this loss. We propose that dimorphic Wg regulation, in concert with monomorphic segment-specific programmed cell death, are the principal mechanisms of sculpting the sexually dimorphic abdomen of Drosophila.morphogenesis | segmentation | homeotic | epithelia B rachycera, higher diptera that include drosophilidae, exhibit an evolutionary trend toward reduced abdominal size that contributes to swift, maneuverable flight (1). Such reduction is especially pronounced within the infraorder Muscomorpha. Within this group of flies, abdominal reduction is sexually dimorphic such that adult males have fewer segments than females. Lower diptera, which includes mosquitoes and midges, retain ancestral morphology with respect to segment number; both adult males and females generate eight abdominal segments. In Muscomorpha the most posterior adult abdominal segments (all or a subset of segments A5-A8) are modified in females, usually as a telescoping ovipositor, whereas corresponding segments are absent in males (2). In all diptera, segment number is monomorphic during embryogenesis and larval development, reflecting the basal insect body plan of three head, three thoracic, and 11 abdominal segments. For most diptera, only embryonic abdominal segments 1-8 generate adult abdominal tissue (only segments 1-7 in the drosophilidae). The more posterior embryonic segments contribute to the adult genitalia. During pupation, sex-specific developmental programs are deployed that sculpt sexually dimorphic segment morphology and number.The posterior abdomen of Drosophila melanogaster serves as an excellent model to study the development of these sex-specific morphologies. Posterior abdominal segment identity, morphology, and number in both sexes is regulated by the Hox protein Abdominal-B (Abd-B) (3, 4). Abd-B ex...