RESUMO
Compartmental boundaries physically separate developing tissues into distinct regions, which is fundamental for the organisation of the body plan in both insects and vertebrates. In many examples, this physical segregation is caused by a regulated increase in contractility of the actomyosin cortex at boundary cell-cell interfaces, a property important in developmental morphogenesis beyond compartmental boundary formation. We performed an unbiased screening approach to identify cell surface receptors required for actomyosin enrichment and polarisation at parasegmental boundaries (PSBs) in early Drosophila embryos, from the start of germband extension at gastrulation and throughout the germband extended stages (stages 6 to 11). First, we find that Tartan is required during germband extension for actomyosin enrichment at PSBs, confirming an earlier report. Next, by following in real time the dynamics of loss of boundary straightness in tartan mutant embryos compared with wild-type and ftz mutant embryos, we show that Tartan is required during germband extension but not beyond. We identify candidate genes that could take over from Tartan at PSBs and confirm that at germband extended stages, actomyosin enrichment at PSBs requires Wingless signalling.
Assuntos
Actomiosina , Proteínas de Drosophila , Animais , Actomiosina/metabolismo , Drosophila/metabolismo , Morfogênese/genética , Proteínas de Drosophila/genética , Proteínas de Drosophila/metabolismoRESUMO
The regionalisation of growing tissues into compartments that do not mix is thought to be a common motif of animal development. Compartments and compartmental boundaries were discovered by lineage studies in the model organism Drosophila. Since then, many compartment boundaries have been identified in developing tissues, from insects to vertebrates. These are important for animal development, because boundaries localize signalling centres that control tissue morphogenesis. Compartment boundaries are boundaries of lineage restriction, where specific mechanisms keep boundaries straight and cells segregated. Here, we review the mechanisms of cell sorting at boundaries found in early Drosophila embryos. The parasegmental boundaries, separating anterior from posterior compartments in the embryo, keep cells segregated by increasing actomyosin contractility at boundary cell-cell interfaces. Differential actomyosin contractility in turn promotes fold formation and orients cell division. Earlier in development, actomyosin differentials are also important for cell sorting during axis extension. Specific cell surface asymmetries and signalling pathways are required to initiate and maintain these actomyosin differentials.
Assuntos
Drosophila melanogaster/citologia , Drosophila melanogaster/embriologia , Embrião não Mamífero/citologia , Morfogênese , Actomiosina/metabolismo , Animais , Divisão Celular , Linhagem da CélulaRESUMO
Several observations in the world of comparative immunology in plants, insects, fish and eventually mammals lead to the discovery of trained immunity in the early 2010's. The first demonstrations provided evidence that innate immune cells were capable of developing memory after a first encounter with some pathogens. Trained immunity in mammals was initially described in monocytes with the Bacille Calmette-Guerin vaccine (BCG) or prototypical agonists like ß-glucans. This phenomenon relies on epigenetic and metabolic modifications leading to an enhanced secretion of inflammatory cytokines when the host encounters homologous or heterologous pathogens. The objective of our research was to investigate the trained immunity, well-described in mouse and human, in other species of veterinary importance. For this purpose, we adapted an in vitro model of trained innate immunity in dogs. Blood enriched monocytes were stimulated with ß-glucans and we confirmed that it induced an increased production of pro-inflammatory and anti-microbial compounds in response to bacterial stimuli. These results constitute the first demonstration of trained immunity in dogs and confirm its signatures in other mammalian species, with an implication of cellular mechanisms similar to those described in mice and humans regarding cellular epigenetics and metabolic regulations.