Alk8 function regulates chamber proportionality. (A–C) Frontal views of hearts from wild-type (A), laf mutant (B) and alk8CA mRNA-injected (C) embryos at 48 h.p.f. Scale bar represents 50 μm. Immunofluorescence detects DsRed (red) in all cardiomyocyte nuclei and atrial myosin heavy chain (Amhc; green) in atrial cells. (A) In a wild-type heart, the ventricle (red) and atrium (green) exhibit typical looping and expansion. (B) In a laf mutant heart, the chambers are unlooped and dysmorphic. (C) In alk8CA mRNA-injected embryos displaying a v2–v3 class of ventralized body morphology (Kishimoto et al., 1997), the hearts are enlarged with a particularly striking expansion of the atrium. (D) Quantification of cardiomyocyte number in wild-type, laf mutant and alk8CA mRNA-injected embryos at 48 h.p.f. Graph indicates the mean and standard deviation for each data set; see also Table S1. Statistically significant differences from wild-type are indicated by asterisks (p < 0.005) or carets (p < 0.05). n = 29 for wild-type, n = 19 for laf mutants, and n = 10 for alk8CA mRNA-injected embryos. laf mutants and alk8CA mRNA-injected embryos have disproportionately small or large atrial chambers, respectively.
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