Damage‐induced regeneration of the intestinal stem cell pool through enteroblast mitosis in the Drosophila midgut

Abstract: Many adult tissues and organs including the intestine rely on resident stem cells to maintain homeostasis and regeneration. In mammals, the progenies of intestinal stem cells (ISCs) can dedifferentiate to generate ISCs upon ablation of resident stem cells. However, whether and how mature tissue cells generate ISCs under physiological conditions remains unknown. Here, we show that infection of the Drosophila melanogaster intestine with pathogenic bacteria induces entry of enteroblasts (EBs), which are ISC progenies, into the mitotic cycle through upregulation of epidermal growth factor receptor (EGFR)‐Ras signaling. We also show that ectopic activation of EGFR‐Ras signaling in EBs is sufficient to drive enteroblast mitosis cell autonomously. Furthermore, we find that the dividing enteroblasts do not gain ISC identity as a prerequisite to divide, and the regenerative ISCs are produced through EB mitosis. Taken together, our work uncovers a new role for EGFR‐Ras signaling in driving EB mitosis and replenishing the ISC pool during fly intestinal regeneration, which may have important implications for tissue homeostasis and tumorigenesis in vertebrates.

Object Details

• Location: Deutsche Nationalbibliothek Frankfurt am Main
• Extent: Online-Ressource
• Language: Englisch

References and Relationships

• Bibliographic citation: Damage‐induced regeneration of the intestinal stem cell pool through enteroblast mitosis in the Drosophila midgut ; day:11 ; month:08 ; year:2022 ; extent:20 ; The EMBO journal / European Molecular Biology Organization ; (11.08.2022) (gesamt 20)

Contributors, Places and Time

• Creator: Tian, Aiguo ; Morejon, Virginia ; Kohoutek, Sarah ; Huang, Yi‐Chun ; Deng, Wu‐Min ; Jiang, Jin

Further information

• DOI: 10.15252/embj.2022110834
• URN: urn:nbn:de:101:1-2022081115262234198779
• Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
• Last update: 12.06.2025, 11:35 AM CEST