Matings among different species of animals or plants often result in sterile or lethal hybrids. Identifying the evolutionary forces that create hybrid incompatibility alleles is fundamental to understanding the process of speciation, but very few such alleles have been identified, particularly in model organisms that are amenable to experimental manipulation. We report here the cloning of the first, to our knowledge, Drosophila melanogaster gene involved in hybrid incompatibilities, Hybrid male rescue (Hmr). Hmr causes lethality and female sterility in hybrids among D. melanogaster and its sibling species. We have found that Hmr encodes a protein with homology to a family of MYB-related DNA-binding transcriptional regulators. The HMR protein has evolved both amino acid substitutions and insertions and deletions at an extraordinarily high rate between D. melanogaster and its sibling species, including in its predicted DNA-binding domain. Our results suggest that hybrid lethality may result from disruptions in gene regulation, and we also propose that rapid evolution may be a hallmark of speciation genes in general.T he process of speciation requires that organisms establish and maintain reproductive isolation from other species. Postzygotic reproductive isolation is widely observed in plants and animals as the sterility and lethality of species hybrids (1). The theory of how such hybrid incompatibilities evolve was proposed independently Ͼ60 years ago by Dobzhansky and Muller (2,3). Their theory envisions that during or after speciation different alleles will evolve in different species. These alleles can reach fixation by either positive selection or neutral drift, but during this period, there is no selection against potentially deleterious interactions with derived alleles that are evolving in other species. These deleterious interactions will be observed only in hybrids between the species.The power of the Dobzhansky͞Muller model derives from its generality. The model can be easily extended to include complex multigene interactions, and it makes no assumptions about the types of genes or allelic changes required to produce incompatibilities. The model is well supported by both theoretical (4) and experimental (1) genetic studies, but only a handful of specific hybrid incompatibility genes have been identified. Without molecular and functional studies of hybrid incompatibility genes, it remains unknown whether particular types of genes or pathways are preferentially involved and what evolutionary processes drive the divergence of these speciation genes.The fruitfly Drosophila melanogaster can hybridize with the closely related species Drosophila simulans, Drosophila mauritiana, and Drosophila sechellia. These three species are estimated to have diverged from D. melanogaster Ϸ2-3 million years ago (5). The cross of D. melanogaster females to males of any of these three sibling species produces F 1 hybrid daughters that are viable but sterile at low temperatures and lethal at high temperatures, whereas F 1 hybr...
Voltage-gated potassium (Kv) channels comprise four transmembrane ␣ subunits, often associated with cytoplasmic  subunits that impact channel expression and function. Here, we show that cell surface expression, voltage-dependent activation gating, and phosphorylation-dependent modulation of Kv2.1 are regulated by cytoplasmic N/C interaction within the ␣ subunit. Kv2.1 surface expression is greatly reduced by C-terminal truncation. Tailless Kv2.1 channels exhibit altered voltage-dependent gating properties and lack the bulk of the phosphorylation-dependent modulation of channel gating. Remarkably, the soluble C terminus of Kv2.1 associates with tailless channels and rescues their expression, function, and phosphorylation-dependent modulation. Soluble N and C termini of Kv2.1 can also interact directly. We also show that the N/C-terminal interaction in Kv2.1 is governed by a 34 aa motif in the juxtamembrane cytoplasmic C terminus, and a 17 aa motif located in the N terminus at a position equivalent to the  subunit binding site in other Kv channels. Deletion of either motif disrupts N/C-terminal interaction and surface expression, function, and phosphorylationdependent modulation of Kv2.1 channels. These findings provide novel insights into intrinsic mechanisms for the regulation of Kv2.1 trafficking, gating, and phosphorylation-dependent modulation through cytoplasmic N/C-terminal interaction, which resembles ␣/ subunit interaction in other Kv channels.
The EnvZ/OmpR two-component regulatory system plays a critical role in the Escherichia coli stress response. In this study, we examined the expression of a new OmpR-regulated gene, ydgR. Our results indicate that ydgR is equivalent to the Salmonella enterica serovar Typhimurium tppB gene and represents a new class of OmpR-regulated genes.
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