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Isolating Intestinal Stem Cells from Adult Drosophila Midguts by FACS to Study Stem Cell Behavior During Aging
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Isolating Intestinal Stem Cells from Adult Drosophila Midguts by FACS to Study Stem Cell Behavior During Aging

Published on: December 16, 2014

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Src kinase function controls progenitor cell pools during regeneration and tumor onset in the Drosophila intestine

A Kohlmaier1, C Fassnacht1, Y Jin1

  • 1Deutsches Krebsforschungszentrum (DKFZ), Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH) Allianz, Im Neuenheimer Feld 282, Heidelberg, Germany.

Oncogene
|July 1, 2014
PubMed

Insights

Src kinases regulate Drosophila intestinal stem cell (ISC) division and tissue growth. Their activation promotes ISC and enteroblast (EB) proliferation, leading to tissue overgrowth and potentially contributing to tumor development.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Cancer Research

Background:

  • Non-receptor tyrosine kinases, particularly Src family kinases, are known to play roles in tumor progression.
  • The Drosophila intestine is a model system for studying tissue homeostasis and regeneration, with intestinal stem cells (ISCs) and enteroblasts (EBs) as key progenitors.

Purpose of the Study:

  • To investigate the role of Src kinases in the Drosophila intestinal stem cell lineage during tissue homeostasis and tumor onset.
  • To understand the mechanisms by which Src kinase activation influences cell cycle progression and tissue overgrowth.

Main Methods:

  • Utilized Drosophila melanogaster as a model organism.
  • Studied the function of Src42a and Src64b kinases in ISC division and tissue regeneration.
  • Investigated the impact of activating Src kinases and Ack on cell cycle progression (G1/S and G2/M phases).
  • Analyzed Stat92E activation and its role in Src-mediated overgrowth.
  • Examined the expression of cell cycle regulators like String/Cdc25 and Cyclin E.

Main Results:

  • Drosophila Src42a and Src64b are essential for optimal regenerative ISC division.
  • Activation of Src kinases (Src42a, Src64b) and Ack promotes the division of quiescent ISCs by driving cell cycle progression.
  • Prolonged Src activation leads to tissue overgrowth via cytokine receptor-independent Stat92E activation.
  • This overgrowth results from the accumulation of weakly specified, division-capable Notch(+) EB-like cells, not increased symmetric ISC division.
  • Src activation induces a mitogenic module (String/Cdc25, Cyclin E), enabling both ISCs and EBs to divide.

Conclusions:

  • Src kinases are critical regulators of ISC and EB proliferation in Drosophila.
  • Src-mediated activation of cell cycle regulators drives tissue overgrowth by expanding intermediate cell populations.
  • These findings offer insights into mechanisms of regenerative growth and tumor development involving stem cell populations and their progenitors.

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