Fig. S1

nrg1^{bns101/bns101} embryos develop a functional heart and survive to adulthood

(a-b) Cartoon of Talen-induced nrg1 mutation with a 14-base-pair deletion in exon 2 (a); this deletion causes a frame shift leading to a premature stop codon in exon 2 resulting in a predicted truncated protein (b). Notably, the predicted truncated Nrg1 protein in nrg1^{bns101/bns101} animals lacks the Ig-like, EGF-like and TM domains that have all been reported to be essential for mouse cardiac trabeculation ^{1, 2, 3}. If the first ATG downstream of the 14 bp deletion is used to reinitiate translation, a protein consisting of part of the TM domain and the carboxy terminal domain will be made. However, the type IIIa Nrg1 isoform 4 is not predicted to be affected by the bns101 mutation. (c-d) nrg1^{bns101/bns101} larvae do not exhibit any gross morphological defects as compared to wild-type; lateral views, anterior to the left; scale bars, 0.5 mm. (e-h) Trabeculation appears unaffected in nrg1^bns101 mutants. 120 hpf larvae from Tg(myl7:LIFEACT-GFP); nrg1^bns101/+ incrosses imaged by spinning disk confocal microscopy; 2D views (mid-sagittal sections) (e and f), and 3D maximum intensity z-projections (g and h); V: ventricle; arrows point to trabecular cardiomyocytes; scale bars, 50 μm.