Referee 1's review:

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N.B. These are the comments made by the referee when reviewing an earlier version of this paper. Prior to publication, the manuscript has been revised in light of these comments and to address other editorial requirements.
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In this report, the authors describe the cloning, expression analysis and effects of morpholino-based gene knockdown of zebrafish mych. This information is novel for zebrafish and, since myc functions in vertebrates generally is incompletely understood and given possibilities for novel functional insights using zebrafish, the paper does report new data that is of interest. The studies in general are performed well with sufficient documentation and quality of analysis. However, there are issues that should be addressed prior to publication listed below.

1) The most puzzling aspect of the interpretation of the data is the focus on neural crest development. While mych is expressed in the arches and early crest regulatory genes are reduced in expression in MO embryos (at least at one timepoint-more should be examined- could simply be a developmental delay), there is ample evidence provided that ectodermal development in general is disrupted. Indeed, analysis of neural plate border development and non-neural ectoderm should be examined. As for the co-expression with foxd3, the figure is unconvincing and would require a section showing this clearly. Similarly, is mych co-expressed with dlx2 in the arches? What is the effect of MO on endodermal and mesodermal populations in the arches? Basically, what is the evidence that mych has any neural crest-specific function? The authors suggest that mych is required for neural crest survival, but while they show increased cell death generally, they provide no evidence that neural crest cells die in morphants. Lastly, I have no idea of what neural crest "maintenance" is and what mych might have to do with it.

2) While mych mRNA rescue of mych morphants provides some evidence of the specificity of the MO used, it would be a much stronger argument (and the quasi norm in zebrafish) to show that another different MO generates the same phenotype and that half-maximal concentrations of each injected together phenocopy each of the single MOs injected at maximal (effective) concentrations.

3) The authors should focus on the role of mych on anterior neuroectoderm patterning and development, defects in which in MO embryos most likely indirectly disrupt anterior neural plate border/crest development.