ZFIN ID: ZDB-FIG-180927-29
Xiao et al., 2018 - The roles of SMYD4 in epigenetic regulation of cardiac development in zebrafish. PLoS Genetics   14:e1007578 Full text @ PLoS Genet.
Observed In:
Stage: Long-pec

Fig. 5

SMYD4 interacts with HDAC1.

(A) Immunofluorescence staining and representative confocal images of the sub-cellular localization of SMYD4 in HL-1 cells. SMYD4 was found in both the nucleus and cytoplasm. The experimental groups without primary anti-SMYD4 antibody incubation served as negative controls; (B) Co-IP/western blotting analysis to confirm the interaction between SMYD4 and HDAC1. SMYD4flag was overexpressed in HL-1 cells. The cell extracts were immunoprecipitated with an anti-FLAG affinity gel, followed by western blotting analysis; (C) The interaction between SMYD4 and HDAC1 was further confirmed by Co-IP/western blotting analysis in HEK293T cells; (D-E) Using a Co-IP/western blotting assay to map the domains in SMYD4 that are responsible for the interaction with HDAC1. The MYND domain of SMYD4 was found to be critical for this interaction; (F) Aberrant histone modifications in MZsmyd4L544Efs*1 embryos at 48 hpf. Specifically, H3K4me2 and H3K4me3 were significantly reduced, and H3K4me was increased, while H3K9me3 and H3K27me3 were not affected, suggesting that SMYD4 is a H3K4-specific methyltransferase. H3K4ac, H3K9ac, H3K14ac, and H3K27ac were significantly abolished in MZsmyd4L544Efs*1 mutants, suggesting the increased activity of HDAC1 in MZsmyd4L544Efs*1 mutants and confirming SMYD4 as an important negative regulator of HDAC1 function; (G) The semi-quantitative analysis of the histone modifications changes in MZsmyd4L544Efs*1 mutants. (p<0.05 *, p<0.01 **).

Gene Expression Details No data available
Antibody Labeling Details No data available
Phenotype Details
Fish Conditions Stage Phenotype
smyd4zf3020/zf3020; zf2036Tg standard conditions Long-pec histone modification process quality, abnormal
Long-pec whole organism H3K4Me3 decreased amount, abnormal
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.