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Midgut Epithelium (midgut + epithelium)
Selected AbstractsProliferation and differentiation of intestinal stem cells during metamorphosis of the red flour beetle, Tribolium castaneumDEVELOPMENTAL DYNAMICS, Issue 4 2008R. Parthasarathy Abstract The insect midgut epithelium is remodeled during larval-pupal metamorphosis when larval polyploid cells (LPCs) are replaced by the daughters of intestinal stem cells (ISCs). We characterized the proliferation of ISCs during midgut remodeling in the red flour beetle, Tribolium castaneum. Midgut remodeling is initiated at 96 hr after ecdysis into the final instar larval stage. Immunocytochemistry with bromodeoxyuridine and phospho-histone H3 antibodies showed that the ISCs are the progenitors of the pupal/adult midgut epithelium and they undergo proliferation and differentiation to form new midgut epithelium. In vitro midgut culture experiments revealed that 20-hydroxyecdysone (20E) in the absence of juvenile hormone induces proliferation of ISCs. RNA interference (RNAi) mediated silencing of ecdysone receptors (EcRA and EcRB) and ultraspiracle (USP) identified EcRA and USP but not EcRB as the proteins involved in 20E regulation of ISCs proliferation. These data show that the proliferation of ISCs is under both developmental and endocrine regulation. Developmental Dynamics 237:893,908, 2008. © 2008 Wiley-Liss, Inc. [source] Fluorescence in situ hybridization (FISH) analysis of the interactions between honeybee larvae and Paenibacillus larvae, the causative agent of American foulbrood of honeybees (Apis mellifera)ENVIRONMENTAL MICROBIOLOGY, Issue 6 2008Dominique Yue Summary American foulbrood (AFB) is a bacterial disease of honeybee larvae caused by the spore-forming bacterium Paenibacillus larvae. Although AFB and its aetiological agent are described now for more than a century, the general and molecular pathogenesis of this notifiable disease is poorly understood. We used fluorescence in situ hybridization (FISH) performed with P. larvae -specific, 16S rRNA-targeted oligonucleotide probes to analyse the early steps in the pathogenesis of American foulbrood. The following chain of events could be demonstrated: (i) the spores germinate in the midgut lumen, (ii) the vegetative bacteria massively proliferate within the midgut before, and (iii) they start to locally breach the epithelium and invade the haemocoel. The paracellular route was shown to be the main mechanism for invasion contrasting earlier hypotheses of phagocytosis of P. larvae. Invasion coincided with the death of the host implicating that the penetration of the midgut epithelium is a critical step determining the time of death. [source] Ultrastructural studies of midgut epithelium formation in Lepisma saccharina L. (Insecta, Zygentoma)JOURNAL OF MORPHOLOGY, Issue 3 2007M. M. Rost-Roszkowska Abstract At the end of embryogenesis of Lepisma saccharina L. (Insecta, Zygentoma), when the stomodaeum and proctodaeum are completely formed, the midgut epithelium is replaced by the primary midgut, a yolk mass is surrounded by a cell membrane. Midgut epithelium formation begins in the 1st larval stage. Energids migrate toward the yolk periphery and aggregate just beneath the cell membrane. They are gradually enclosed by cell membrane folds of the primary midgut. Single cells are formed. Succeeding energids join just formed cells. Thus, groups of cells, regenerative cell groups, are formed. Their number gradually increases. The external cells of the regenerative cell groups transform into epithelial cells and their basal regions spread toward the next regenerative cell groups. Epithelial cells of neighboring regenerative cell groups join each other to form the epithelium. At the end of the 2nd larval stage, just before molting, degeneration of newly the formed epithelium begins. Remains of organelles and basal membrane occur between the regenerative cell groups. The new epithelium is formed from the regenerative cell groups, which are now termed stem cells of the midgut epithelium. J. Morphol., 2007. © 2007 Wiley-Liss, Inc. [source] Factors affecting proliferation and differentiation of lepidopteran midgut stem cells,ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 1 2010Marcia J. Loeb Midgut stem cells of last instar larvae and pupae of Heliothis virescens, Lymantria dispar and several other Lepidopteran species have been cultured in vitro and have been induced to proliferate using low titers of ecdysteroids and the 77-Kda peptide fragment, ,-arylphorin, isolated and identified from pupal fat body tissue. The insulin-related hormone, Bombyxin, also induced mitosis in cultured midgut stem cells; it appeared to be fast-acting and quickly inactivated, while ,-arylphorin was slower to act and had a longer lasting effect in vitro, indicating different functions for these proliferation agents. Changes in Calcium ion concentration within or outside the cells discretely affected stem cell differentiation, indicating a role for second messenger participation in peptide regulation of this process. Four different peptides (MDFs 1,4) that induced midgut stem cells to differentiate to mature midgut cell types in vitro were isolated and characterized from conditioned media and hemolymph of H. virescens and L. dispar. However, platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and all-trans retinoic acid (RA) from vertebrate sources induced differentiation to non-midgut cell types as well. MDF1 was located in basal areas of columnar cells of midgut epithelium, although MDF2 was observed in all of the cytoplasm of columnar cells and in droplets of antibody positive material in the midgut lumen, suggesting a digestive function as well for this peptide. Anti-MDF-3 stained the central areas of cultured midgut columnar cells and the bases of columnar cells of midgut epithelium in vivo. Midgut secretory cells stained with anti-MDF-4; streams of MFD-4-positive material were observed extending from secretory cells facing the epithelial lumen, and as a layer on the hemolymph-facing side, suggesting an endocrine or paracrine function for this or an immunologically similar peptide. Published 2010 Wiley Periodicals, Inc. [source] Bacterial infection of a model insect: Photorhabdus luminescens and Manduca sextaCELLULAR MICROBIOLOGY, Issue 6 2002Carlos P. Silva Summary Invertebrates, including insects, are being developed as model systems for the study of bacterial virulence. However, we understand little of the interaction between bacteria and specific invertebrate tissues or the immune system. To establish an infection model for Photorhabdus, which is released directly into the insect blood system by its nematode symbiont, we document the number and location of recoverable bacteria found during infection of Manduca sexta. After injection into the insect larva, P. luminescens multiplies in both the midgut and haemolymph, only later colonizing the fat body and the remaining tissues of the cadaver. Bacteria persist by suppressing haemocyte-mediated phagocytosis and culture supernatants grown in vitro, as well as plasma from infected insects, suppress phagocytosis of P. luminescens. Using GFP-labelled bacteria, we show that colonization of the gut begins at the anterior of the midgut and proceeds posteriorly. Within the midgut, P. luminescens occupies a specific niche between the extracellular matrix and basal membrane (lamina) of the folded midgut epithelium. Here, the bacteria express the gut-active Toxin complex A (Tca) and an RTX-like metalloprotease PrtA. This close association of the bacteria with the gut, and the production of toxins and protease, triggers a massive programmed cell death of the midgut epithelium. [source] | ||||||||||