Fig. S3
Fig. S3 Lysyl oxidase and collagen II splice morpholinos decrease the abundance of wild-type splice forms and cause specific changes in splice site usage. (A) loxl1, (B) loxl2b, (C) loxl3b, (D) loxl5b and (E) col2a1. Wild-type embryos injected with the indicated doses of morpholino were harvested at 20 hpf and cDNA prepared from equal amounts of RNA. The intensity of the wild-type (WT) product obtained by PCR was quantified and the percentage of wild-type splice form remaining after morpholino knockdown determined, as noted. This measure is independent of processes that may depress levels of the mutant (Mut) splice products, including degradation through nonsense-mediated decay. The primer set used to amplify loxl1 does not amplify the mutant band.
Reprinted from Developmental Biology, 307(2), Gansner, J.M., Mendelsohn, B.A., Hultman, K.A., Johnson, S.L., and Gitlin, J.D., Essential role of lysyl oxidases in notochord development, 202-213, Copyright (2007) with permission from Elsevier. Full text @ Dev. Biol.