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

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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:	twu34Tg + MO2-smarcc1a twu34Tg + MO3-smarcc1a
Knockdown Reagents:	MO2-smarcc1a MO3-smarcc1a
Observed In:	heart heart morphogenesis
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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