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Ocaña, O. H. et al. A right-handed signalling pathway drives heart looping in vertebrates. Nature 549, 86–90 (2017).
Barske, L. et al. Competition between Jagged-Notch and Endothelin1 signaling selectively restricts cartilage formation in the zebrafish upper face. PLoS Genet. 12, e1005967 (2016).
Blum, M., Feistel, K., Thumberger, T. & Schweickert, A. The evolution and conservation of left–right patterning mechanisms. Development 141, 1603–1613 (2014).
Ocaña, O. H. et al. Metastatic colonization requires the repression of the epithelial-mesenchymal transition inducer Prrx1. Cancer Cell 22, 709–724 (2012).
Heasman, J. Morpholino oligos: making sense of antisense? Dev. Biol. 243, 209–214 (2002).
Kok, F. O. et al. Reverse genetic screening reveals poor correlation between morpholino-induced and mutant phenotypes in zebrafish. Dev. Cell 32, 97–108 (2015).
Law, S. H. & Sargent, T. D. The serine-threonine protein kinase PAK4 is dispensable in zebrafish: identification of a morpholino-generated pseudophenotype. PLoS One 9, e100268 (2014).
Stainier, D. Y. R. et al. Guidelines for morpholino use in zebrafish. PLoS Genet. 13, e1007000 (2017).
Gentsch, G.E. et al. Innate immune response and off-target mis-splicing are common morpholino-induced side effects in Xenopus. Dev. Cell 44, 597–610 (2018).
Joris, M. et al. Number of inadvertent RNA targets for morpholino knockdown in Danio rerio is largely underestimated: evidence from the study of Ser/Arg-rich splicing factors. Nucleic Acids Res. 45, 9547–9557 (2017).
Anderson, J. L. et al. mRNA processing in mutant zebrafish lines generated by chemical and CRISPR-mediated mutagenesis produces unexpected transcripts that escape nonsense-mediated decay. PLoS Genet. 13, e1007105 (2017).
Rossi, A. et al. Genetic compensation induced by deleterious mutations but not gene knockdowns. Nature 524, 230–233 (2015).
El-Brolosy, M. A. et al. Genetic compensation triggered by mutant mRNA degradation. Nature 568, 193–197 (2019).
Ma, Z. et al. PTC-bearing mRNA elicits a genetic compensation response via Upf3a and COMPASS components. Nature 568, 259–263 (2019).
Hwang, W. Y. et al. Efficient genome editing in zebrafish using a CRISPR–Cas system. Nat. Biotechnol. 31, 227–229 (2013).
We acknowledge support from the Dutch Heart Foundation grant CVON2014-18 CONCOR-GENES to J.B. and the National Institute of Health grants NIH R35 DE027550 to J.G.C., NIH R00 DE024190 to J.T.N. (National Institute of Dental and Craniofacial Research, NIDCR) and NIH R00 DE026239 to L.B. (NIDCR).
The authors declare no competing interests.
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Tessadori, F., de Bakker, D.E.M., Barske, L. et al. Zebrafish prrx1a mutants have normal hearts. Nature 585, E14–E16 (2020). https://doi.org/10.1038/s41586-020-2674-1