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First published online 20 August 2003
doi: 10.1242/dev.00691
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1 Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern
University, Evanston, IL 60208, USA
2 Division of Neurosciences, Beckman Research Institute of the City of Hope,
Duarte, CA 91010, USA
Author for correspondence (e-mail:
beitel{at}northwestern.edu)
Accepted 16 June 2003
Although the correct architecture of epithelial tubes is crucial for the
function of organs such as the lung, kidney and vascular system, little is
known about the molecular mechanisms that control tube size. We show that
mutations in the ATP
and nrv2 ß subunits
of the Na+/K+ ATPase cause Drosophila tracheal
tubes to have increased lengths and expanded diameters. ATP
and nrv2 mutations also disrupt stable formation of septate
junctions, structures with some functional and molecular similarities to
vertebrate tight junctions. The Nrv2 ß subunit isoforms have unique tube
size and junctional functions because Nrv2, but not other Drosophila
Na+/K+ ATPase ß subunits, can rescue nrv2
mutant phenotypes. Mutations in known septate junctions genes cause the same
tracheal tube-size defects as ATP and nrv2 mutations,
indicating that septate junctions have a previously unidentified role in
epithelial tube-size control. Double mutant analyses suggest that tube-size
control by septate junctions is mediated by at least two discernable pathways,
although the paracellular diffusion barrier function does not appear to
involved because tube-size control and diffusion barrier function are
genetically separable. Together, our results demonstrate that specific
isoforms of the Na+/K+ ATPase play a crucial role in
septate junction function and that septate junctions have multiple distinct
functions that regulate paracellular transport and epithelial tube size.
Key words: Tracheal system, Na+/K+ ATPase, Na+ pump, Septate junctions, Tight junctions, Epithelial tubes, Epithelial morphogenesis, Tube-size control, Tubulogenesis, Drosophila
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