Fig 7. Hapln1a and Sema3d interact genetically to mediate Cx43 phenotypes.

Prior to knockdown and electroporation, all fins were amputated at 50% level and allowed to regenerate for 3 days. Fin rays treated with combined targeting MO or combined control MM were measured and compared to their un-injected sides. The ratio of injected (MO or control MO) and un-injected side multiplied by 100 is the percent similarity. Percent similarity greater than 100% reflects the fact that the experimental side can be measurably larger than the control un-injected side. Independent hapln1a knockdown at 0.5mM concentration and sema3d knockdown at 0.25mM concentration did not produce significant effects on Cx43 dependent phenotypes (not shown). Bar graphs reveal that double knockdown at MO concentrations of 0.5mM Hapln1a and 0.25mM of Sema3d recapitulated the Cx43 knockdown phenotypes (reduced regenerate length, segment length and cell proliferation), suggesting that Hapln1a and Sema3d interact genetically to promote Cx43 function. Students t-test was performed (p<0.05) to determine significance, and the error bars indicate standard error of the mean.