FIGURE

Fig. S1

ID
ZDB-FIG-190108-8
Publication
Cantù et al., 2018 - Mutations in Bcl9 and Pygo genes cause congenital heart defects by tissue-specific perturbation of Wnt/β-catenin signaling.
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Fig. S1

MZbcl9l∆4 mutants are viable and fertile.

(A,B) Schematics showing the mutation induced in bcl9l∆4 mutants. Analogous to bcl9 mutants (see Figure 1B,C), we designed a sgRNA that induces mutagenesis between the HD1 and HD2 domain. Gene locus represented as per genome annotation Zv10 (A) with two isoforms that differ in the first coding exon and the untranslated regions (UTRs). The green dotted box represents a zoomed region of the gene locus, with the red line representing the location of the sgRNA used for mutagenesis; black boxes mark coding exons (CDS), white boxes mark UTRs, the blue boxes represent the part of the CDS that will contribute to HD1 and purple boxes to HD2. A 4 bp deletion at the Cas9 cutting side (B) leads to a frame-shift allele with a premature STOP codon before HD2. (C-G) Brightfield images of homozygous bcl9l∆4 mutants at different stages from gastrulation to adulthood, lateral views, anterior to the left. Maternal zygotic bcl9l mutants (MZbcl9l∆4) mutants did not show any gastrulation defects (C,D). At 5 dpf, we could not detect any cardiac and craniofacial phenotypes (E,F) as observed in zygotic bcl9∆29 mutants (see Figure 1). (G) Representative image of a five-month old (5 mo) MZbcl9l∆4 F4 mutant obtained from a cross of two adult homozygous bcl9l∆4 mutants. Scale bars, 500 µm.

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data

Phenotype Detail
Acknowledgments
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