Stephen L Johnson

In the 2006 paper on jaguar/obelix zebrafish, the authors note that connexin41.8 was identified as the gene responsible for the leopard phenotype. They add that its product takes part in both hemichannel and intercellular channel formation. The citation is to T. Chen and S. L. Johnson, as personal communication¹. The authors suggest that small molecules passing through such channels may contribute to pattern formation. The same paper, on which Johnson is a co-author, predicted that loss of the Kir7.1 channel would disturb melanophore responses to external signals².

Johnson is a co-author of the 2014 paper on size control in zebrafish fins. It places its mutant, in the kcnk5b potassium channel gene, within a growing body of evidence that bioelectrical signals orchestrate patterning and growth⁴. They stress that the overgrown structures kept their organisation, so the result is not simple tumorous overgrowth.

The 2018 paper, also co-authored by Johnson, starts from the finding that blocking calcineurin with FK506 or cyclosporin A enlarges fins⁵. The authors then tested fish lacking kcnk5b. In these fish the growth response to FK506 was suppressed. They concluded that Kcnk5b is a critical component of FK506-mediated regulation of growth and size⁶. Some extra growth remained, which they attributed possibly to the kcnk5a paralogue or other FK506 targets.