Zebrafish prrx1a mutants have normal hearts

[No abstract; first paragraph shown] How organ laterality is established during embryo development is an intriguing question that remains largely unresolved. By using morpholino-based knockdown and CRISPR–Cas9-induced somatic mutations in zebrafish embryos, Ocaña et al.1 reported a role for the paired-like homeobox transcription factor Prrx1a in a novel right-handed signalling pathway that drives cardiac looping. We analysed this process in two previously described frameshift prrx1a-mutant alleles2, as well as in three newly generated large-deletion alleles that remove exon 1 and upstream sequences around the transcriptional start site (TSS), or the entire locus of the prrx1a gene such that no mRNA is produced. Homozygosity of any of these five alleles does not affect cardiac looping, which calls into question the requirement for prrx1a in left–right (L–R) patterning and cardiac development.