J Membrane Biol (2013) 246:665–667 DOI 10.1007/s00232-013-9585-0 LETTE R T O T HE EDI T OR Response to ‘‘What Do Aquaporin Knockout Studies Tell Us about Fluid Transport in Epithelia?’’ Maclaren OJ, Sneyd J, Crampin EJ (2013) J Membr Biol 246:297–305 A. E. Hill Y. Shachar-Hill Received: 31 July 2013 / Accepted: 4 August 2013 / Published online: 22 August 2013 Springer Science+Business Media New York 2013 Dear Sir, untrue; and (3) that their claim that a basis for this effect Epithelial isotonic ﬂuid transport was originally assumed to can be found in a recent article of theirs in this journal be based upon osmotic equilibration following active salt (Maclaren et al. 2012) is unsupported. transport, and with the discovery of aquaporins (AQPs) The authors repeatedly comment on our failure to real- present in epithelial membranes and dominating the osmotic ize the ‘‘nonlinearity’’ of the problem, meaning that we permeability, it became apparent that genetic knockout (KO) assume a reduction in osmotic permeability should be of these would be a speciﬁc test of the osmotic theory. Such reﬂected in a proportional reduction in ﬂuid ﬂow; we do experiments were conducted for several AQPs in water not, but linearity had
The Journal of Membrane Biology – Springer Journals
Published: Aug 22, 2013
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