Journal
JOURNAL OF CELL SCIENCE
Volume 119, Issue 5, Pages 846-857Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.02807
Keywords
Kazal domain; SPINK1/SPINK3 serine protease inhibitor; autophagy; autophagosome; RNA interference; evolution
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In hydra, the endodermal epithelial cells carry out the digestive function together with the gland cells that produce zymogens and express the evolutionarily conserved gene Kazall. To assess the hydra Kazall function, we silenced gene expression through double-stranded RNA feeding. A progressive Kazall silencing affected homeostatic conditions as evidenced by the low budding rate and the induced animal death. Concomitantly, a dramatic disorganization followed by a massive death of gland cells was observed, whereas the cytoplasm of digestive cells became highly vacuolated. The presence of mitochondria and late endosomes within those vacuoles assigned them as autophagosomes. The enhanced Kazall expression in regenerating tips was strongly diminished in Kazal1(-) hydra, and the amputation stress led to an immediate disorganization of the gland cells, vacuolization of the digestive cells and death after prolonged silencing. This first cellular phenotype resulting from a gene knockdown in cnidarians suggests that the Kazal1 serine-protease-inhibitor activity is required to prevent excessive autophagy in intact hydra and to exert a cytoprotective function to survive the amputation stress. Interestingly, these functions parallel the pancreatic autophagy phenotype observed upon mutation within the Kazal domain of the SPINK1 and SPINK3 genes in human and mice, respectively.
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