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<p>The growth and tissue turnover in the adult <i>Drosophila melanogaster</i> midgut, mediated by intestinal stem cells (ISCs), is well-established, but the process in the larval gut remains unclear. The present accepted hypothesis assumes that larval midgut cells remain persistent throughout the larval period and growth of the midgut is a result of endoreplication of enterocytes (ECs). In contrast to this view, we observed that the larval midgut grows as a result of an increase in both cell number and size, based on 4’,6-diamidino-2-phenylindole (DAPI) staining, Propidium Iodide (PI) staining for cell death, Phosphorylated-histone H3 (Phosphohistone-H3) staining for mitotic activity, and 5-bromo-2'-deoxyuridine (BrdU) incorporation studies. Furthermore, in contrast to the previous hypothesis, we show that inducing stress with Dextran Sulfate Sodium (DSS) leads to midgut cell death in 2nd instar, initiating the process of replenishment of Enteroblasts (both ECs and Eneteroendocrine cells) in the 3rd instar midgut. Thus, in contrast with earlier reports, our results show that larval midgut is not a persistent entity and that the cells laid in the embryonic stage are replaced and replenished with a new cell population wherein larval midgut cells increase at a constant rate following a linear trend during normal development and under stress.</p>

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Drosophila melanogaster larval midgut remodeling during development and damage

  • 期刊论文

  • 发表日期：

    2025年10月28日

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  • Ambika Singh,
  • Rajagopal Raman

摘要

The growth and tissue turnover in the adult Drosophila melanogaster midgut, mediated by intestinal stem cells (ISCs), is well-established, but the process in the larval gut remains unclear. The present accepted hypothesis assumes that larval midgut cells remain persistent throughout the larval period and growth of the midgut is a result of endoreplication of enterocytes (ECs). In contrast to this view, we observed that the larval midgut grows as a result of an increase in both cell number and size, based on 4’,6-diamidino-2-phenylindole (DAPI) staining, Propidium Iodide (PI) staining for cell death, Phosphorylated-histone H3 (Phosphohistone-H3) staining for mitotic activity, and 5-bromo-2'-deoxyuridine (BrdU) incorporation studies. Furthermore, in contrast to the previous hypothesis, we show that inducing stress with Dextran Sulfate Sodium (DSS) leads to midgut cell death in 2nd instar, initiating the process of replenishment of Enteroblasts (both ECs and Eneteroendocrine cells) in the 3rd instar midgut. Thus, in contrast with earlier reports, our results show that larval midgut is not a persistent entity and that the cells laid in the embryonic stage are replaced and replenished with a new cell population wherein larval midgut cells increase at a constant rate following a linear trend during normal development and under stress.