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Living organisms experience tissue damage from both, the surrounding environment and from inside their bodies. Tissue repair/regeneration is triggered by local tissue injury to restore an injured, or lost, part of the body. Tissue damage results in a series of responses, not only locally but also systemically in distant tissues. In our recent publication, we established a "dual system" that induces spatiotemporal tissue damage simultaneously with gene manipulation in surrounding tissues. With this system, we demonstrated that appropriate regulation of methionine metabolism in the fat body is required for tissue repair in Drosophila wing discs, thus highlighting the importance of systemic damage response (SDR) in tissue repair. This "Extra View" aims to discuss our recent reports that propose methionine metabolism to be an essential part of SDR, together with related topics in several model organisms.

A full understanding of how ecological factors drive the fixation of genetic changes during speciation is obscured by the lack of appropriate models with clear natural history and powerful genetic toolkits. In a recent study, we described an early stage of ecological speciation in a population of the generalist species Drosophila yakuba (melanogaster subgroup) on the island of Mayotte (Indian Ocean). On this island, flies are strongly associated with the toxic fruits of noni (Morinda citrifolia) and show a partial degree of pre-zygotic reproductive isolation. Here, I mine the nuclear and mitochondrial genomes and provide a full morphological description of this population. Only 29 nuclear sites (< 4 × 10^-7 of the genome) are fixed in this population and absent from 3 mainland populations and the closest relative D. santomea, but no mitochondrial or morphological character distinguish Mayotte flies from the mainland. This result indicates that physiological and behavioral traits may evolve faster than morphology at the early stages of speciation. Based on these differences, the Mayotte population is designated as a new subspecies, Drosophila yakuba mayottensis subsp. nov., and its strong potential in understanding the genetics of speciation and plant-insect interactions is discussed.

Apoptosis-induced proliferation (AiP) maintains tissue homeostasis following massive stress-induced cell death. During this phenomenon, dying cells induce proliferation of the surviving cells to compensate for the tissue loss, and thus restore organ size. Along with wound healing and tissue regeneration, AiP also contributes to tumor repopulation following radiation or chemotherapy. There are several models of AiP. Using an "undead" AiP model that causes hyperplastic overgrowth of Drosophila epithelial tissue, we recently demonstrated that extracellular reactive oxygen species (eROS) are produced by undead epithelial cells, and are necessary for inducing AiP and overgrowth. Furthermore, hemocytes, the Drosophila blood cells, are seen adjacent to the undead epithelial tissue, and may secrete the TNF ortholog Eiger that signals through the TNF receptor to active Jun-N-terminal kinase (JNK) in the undead tissue and induce proliferation. We propose that undead epithelial tissue triggers an inflammatory response that resembles recruitment of macrophages to human epithelial tumors, and that these tumor-associated macrophages release signals for proliferation and tumor growth of the epithelium. This Extra View article summarizes these recent findings with a focus on the role of eROS for promoting regeneration and inflammation-induced tumorigenesis.