Larval terminal cells of the Drosophila tracheal system generate extensive branched tubes, requiring a huge increase in apical membrane. We discovered that terminal cells compromised for apical membrane expansion – mTOR-vATPase axis and apical polarity mutants – were invaded by the neighboring stalk cell. The invading cell grows and branches, replacing the original single intercellular junction between stalk and terminal cell with multiple intercellular junctions . Here we characterize disjointed, a mutation in the same phenotypic class. We find that disjointed encodes Drosophila Archease, required for RNA ligase (RtcB) function critical for tRNA maturation and ER stress-regulated nonconventional splicing of Xbp1 mRNA. We show that the steady-state subcellular localization of Archease is principally nuclear, and dependent upon TOR-vATPase activity. In tracheal cells mutant for Rheb or vATPase, Archease localization shifted dramatically from nucleus to cytoplasm. Further, we found that blocking tRNA maturation by knockdown of tRNAse z also induced compensatory branching. Taken together, these data suggest that the TOR-vATPase axis promotes apical membrane growth in part through nuclear localization of Archease, where Archease is required for tRNA maturation.
Regulation of Archease by the mTOR-vATPase axis
Present address: James Cook University, 1 James Cook Dr, Douglas QLD 4811, Australia
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- Funder(s): National Institutes of Health
- Award Id(s): GM089782
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Deanne Francis, Alondra S. Burguete, Amin Ghabrial; Regulation of Archease by the mTOR-vATPase axis. Development 2022; dev.200908. doi: https://doi.org/10.1242/dev.200908
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