Related Experiment Video
Updated: Jul 7, 2025

10:57
Isolating Intestinal Stem Cells from Adult Drosophila Midguts by FACS to Study Stem Cell Behavior During Aging
Published on: December 16, 2014
20.5K
Host-Microbe Interactions Regulate Intestinal Stem Cells and Tissue Turnover in Drosophila
Ji-Hoon Lee1,2
1National Creative Research Initiative Center for Hologenomics and School of Biological Sciences, Seoul National University, Seoul, Korea.
International Journal of Stem Cells
|December 20, 2023
Summary
The study reveals how gut microbes and pathogens regulate intestinal stem cell activity and tissue turnover in Drosophila. This interaction is key to maintaining gut health and epithelial homeostasis.
Area of Science:
- * Developmental Biology
- * Immunology
- * Microbiology
Background:
- * The gut epithelium is a dynamic tissue requiring continuous renewal via intestinal stem cells.
- * Drosophila melanogaster is a powerful model for studying stem cell regulation due to its conserved gut structure and available genetic tools.
- * The gut epithelium constantly interacts with microbes and pathogens, necessitating immune responses and tissue turnover.
Purpose of the Study:
- * To explore the role of gut microbes and pathogens in regulating intestinal stem cell proliferation and differentiation.
- * To elucidate the interplay between the host innate immune system and the gut microbiome in maintaining epithelial homeostasis.
Main Methods:
- * Utilized Drosophila as a model organism.
- * Leveraged advanced genetic and histologic techniques.
- * Investigated the effects of microbial and pathogen exposure on the gut epithelium.
Main Results:
- * Microbiome and pathogens are significant regulators of intestinal tissue turnover.
- * Interactions between gut microbes and the host innate immune system influence stem cell behavior.
- * These interactions are critical for maintaining intestinal stem cell proliferation and differentiation.
Conclusions:
- * Gut microbes and pathogens play a crucial role in regulating intestinal stem cell activity.
- * The innate immune system's interaction with the gut microbiome is vital for epithelial homeostasis.
- * Understanding these dynamics in Drosophila provides insights into gut health regulation.
Related Concept Videos
Role Of Notch Signalling In Intestinal Stem Cell Renewal
2.1K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.1K
Renewal of Intestinal Stem Cells
2.6K
The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
2.6K
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
2.2K
Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
2.2K

