FIGURE

Fig. S6

ID
ZDB-FIG-170914-32
Publication
Scott et al., 2017 - Nuclear/cytoplasmic transport defects in BBS6 underlie congenital heart disease through perturbation of a chromatin remodeling protein
Other Figures
All Figure Page
Back to All Figure Page
Fig. S6

Smarcc1a knockout/knockdown causes cardiac phenotypes.

Attempts to generate smarcc1a knockout zebrafish are unsuccessful because smarcc1a heterozygous fish, in the F1 generation, do not survive to breeding age (A). Smarcc1a knockdown with a translation blocking (ATG) morpholino (MO) causes multiple development phenotypes in the zebrafish in a dose dependent manner; phenotypes match smarcc1a heterozygous mutants (B). Heart labeled using transgenic line expressing GFP in differentiated cardiac tissue, Tg(myl7:EGFP) (C). Western blot for total protein validating that a human SMARCC1 antibody cross-reacts with zebrafish smarcc1a; reduced levels are observed in smarcc1a knockdown (0.5ng of MO) embryos compared to control MO injected embryos; Actin was used as a control (D). Percent of zebrafish larvae displaying cardiovascular defects from control MO, smarcc1a ATG MO, smarcc1a splice block MO, and smarcc1a splice block MO + smacc1a mRNA; fishers exact test used to compare groups, p-values: * < 0.05, **** <0.0001 (E).

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data
Fish:
Knockdown Reagents:
Observed In:
Stage: Long-pec

Phenotype Detail
Acknowledgments
This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image. Full text @ PLoS Genet.