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Proper control of adult stem cells including their proliferation and differentiation is crucial in maintaining homeostasis of well-organized tissues/organs throughout an organism's life. The  Drosophila  adult midgut has intestinal stem cells (ISCs), which have been exploited as a simple model system to investigate mechanisms controlling adult tissue homeostasis. Here, we found that a viable mutant of  βν integrin  ( βint-ν ), encoding one of two  Drosophila  integrin β subunits, showed a short midgut and abnormal multilayered epithelia accompanied by an increase in ISC proliferation and misdifferentiation defects. The increase in ISC proliferation and misdifferentiation was due to frequent ISC duplication expanding a pool of ISCs, which was caused by depression of the Notch signalling, and up-regulation of  unpaired  ( upd ), a gene encoding an extracellular ligand in the JAK/STAT signalling pathway. In addition, we observed that abnormally high accumulation of filamentous actin (F-actin) was caused in the  βint-ν  mutant enterocytes. Furthermore, the defects were rescued by suppressing c-Jun N-terminal kinase (JNK) signalling, which was up-regulated in a manner correlated with the defect levels in the above-mentioned  βint-ν  mutant phenotype. These symptoms observed in young  βint-ν  mutant midgut were very similar to those in the aged midgut in wild type. Our results suggested that  βint-ν  has a novel function for the  Drosophila  adult midgut homeostasis under normal conditions and provided a new insight into possible age-related diseases caused by latent abnormality of an integrin function.

βν Integrin Inhibits Chronic and High Level Activation of JNK to Repress Senescence Phenotypes in Drosophila Adult Midgut