header logo image header logo text
Downloads Login
Research
General Information
ZIRC
ZFIN ID: ZDB-FIG-170914-32
Scott et al., 2017 - Nuclear/cytoplasmic transport defects in BBS6 underlie congenital heart disease through perturbation of a chromatin remodeling protein. PLoS Genetics   13:e1006936 Full text @ PLoS Genet.
ADDITIONAL FIGURES
PHENOTYPE:
Fish:
Knockdown Reagents:
Observed In:
Stage: Long-pec

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).

Gene Expression DetailsNo data available
Antibody Labeling Details No data available
Phenotype Details
Fish Conditions Stage Phenotype
twu34Tg + MO2-smarcc1a standard conditions Long-pec heart morphology, abnormal
Long-pec heart morphogenesis disrupted, abnormal
twu34Tg + MO3-smarcc1a standard conditions Long-pec heart morphology, abnormal
Long-pec heart morphogenesis disrupted, abnormal
Acknowledgments:
ZFIN wishes to thank the journal PLoS Genetics for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ PLoS Genet.