No abstract

The Drosophila intestine is maintained by multipotent intestinal stem cells (ISCs). Although increased intestinal stem cell (ISC) proliferation has been correlated with a decrease in longevity, there is some discrepancy regarding whether a decrease or block in proliferation also has negative consequences. Here we identify headcase (hdc) as a novel marker of ISCs and enteroblasts (EBs) and demonstrate that Hdc function is required to prevent ISC/EB loss through apoptosis. Hdc depletion was used as a strategy to ablate ISCs and EBs in order to test the ability of flies to survive without ISC function. While flies lacking ISCs showed no major decrease in survival under unchallenged conditions, flies depleted of ISCs and EBs exhibited decreased survival rates in response to damage to mature enterocytes (EC) that line the intestinal lumen. Our findings indicate that constant renewal of the intestinal epithelium is not absolutely necessary under normal laboratory conditions, but it is important in the context of widespread chemical-induced damage when significant repair is necessary.

Hedgehog (HH) signaling is an intercellular communication pathway involved in directing the development and homeostasis of metazoans. HH signaling depends on lipids that covalently modify HH proteins and participate in signal transduction downstream. In many animals, the HH pathway requires the primary cilium, an organelle with a specialized protein and lipid composition. Here, we review the intimate connection between HH signaling and lipids. We highlight how lipids in the primary cilium can create a specialized microenvironment to facilitate signaling, and how HH and components of the HH signal transduction pathway use lipids to communicate between cells.