Stem cell aging is controlled both intrinsically and extrinsically in the Drosophila ovary

Cell Stem Cell. 2007 Oct 11;1(4):458-69. doi: 10.1016/j.stem.2007.09.010.


It is widely postulated that tissue aging could be, at least partially, caused by reduction of stem cell number, activity, or both. However, the mechanisms of controlling stem cell aging remain largely a mystery. Here, we use Drosophila ovarian germline stem cells (GSCs) as a model to demonstrate that age-dependent decline in the functions of stem cells and their niche contributes to overall stem cell aging. BMP signaling activity from the niche significantly decreases with age, and increasing BMP signaling can prolong GSC life span and promote their proliferation. In addition, the age-dependent E-cadherin decline in the stem cell-niche junction also contributes to stem cell aging. Finally, overexpression of SOD, an enzyme that helps eliminate free oxygen species, in either GSCs or their niche alone can prolong GSC life span and increase GSC proliferation. Therefore, this study demonstrates that stem cell aging is controlled extrinsically and intrinsically in the Drosophila ovary.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Morphogenetic Proteins / metabolism
  • Cadherins / metabolism
  • Cell Count
  • Cell Proliferation
  • Cellular Senescence*
  • Drosophila melanogaster / cytology*
  • Female
  • Models, Biological
  • Ovary / cytology*
  • Ovary / enzymology
  • Ovum / cytology
  • Ovum / enzymology
  • Signal Transduction
  • Stem Cells / cytology*
  • Superoxide Dismutase / metabolism
  • Time Factors


  • Bone Morphogenetic Proteins
  • Cadherins
  • Superoxide Dismutase