Focal Point Christopher Koehler, Leanne Jones, and colleagues demonstrate that Drosophila intestinal stem cells (ISCs) unable to degrade damaged mitochondria via the process of mitophagy can enter a senescence-like state where they are unable to proliferate. Compared with wild-type cells (left), ISCs lacking the key mitophagy proteins Pink1 (center) or Parkin (right) accumulate dysfunctional mitochondria with abnormal morphologies. These damaged mitochondria produce elevated levels of reactive oxygen species, which typically trigger ISC proliferation, a hallmark of intestinal aging. However, because loss of pink1 or parkin suppresses ISC proliferation by inducing senescence, intestinal aging is delayed. Photos courtesy of the authors.

Focal Point Christopher Koehler, Leanne Jones, and colleagues demonstrate that Drosophila intestinal stem cells (ISCs) unable to degrade damaged mitochondria via the process of mitophagy can enter a senescence-like state where they are unable to proliferate. Compared with wild-type cells (left), ISCs lacking the key mitophagy proteins Pink1 (center) or Parkin (right) accumulate dysfunctional mitochondria with abnormal morphologies. These damaged mitochondria produce elevated levels of reactive oxygen species, which typically trigger ISC proliferation, a hallmark of intestinal aging. However, because loss of pink1 or parkin suppresses ISC proliferation by inducing senescence, intestinal aging is delayed. Photos courtesy of the authors.

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