Referee 1's review:


Review of the original submission of the manuscript:

This is a well performed study, which has given an extensive description on the defects in the dispersal of cerebellar Purkinje neurons caused by mutation of the reelin receptors APOER2 and VLDLR. Images are presented in very high quality and results are very clear. The authors have discussed potential mechanisms underlying the observed phenotype, however, did not perform any experiments to test these possibilities. It's highly recommended that the authors perform experiments to address the following questions:

1. Does the selective ectopia of Purkinje neurons correlate with the expression level of these two receptors in corresponding neurons? Extensive study is required to examine the developmental expression profile of these two receptors in different domains of cerebellum. The authors can also consider to generate mice with the transgenic labeling of VLDLR-expressing neurons and APOER2-expressing neurons and cross these mouse lines with the mutant to visualize the positioning of each group of neurons in wide type and in mutant animals.
2. What's the relation between these two receptors? Do they play identical and synergistic functions during the Purkinje cell dispersal, or play divergent roles like these receptors do during the cortical radial migration (Development 134, 3883-3891 (2007))? Do they compensate each other in single mutant animals? Can the defects of Purkinje neuron dispersal in one mutant be rescued by transgenic overexpression of another?


Review of the first revised manuscript:

In this revised manuscript, the authors made additional discussions in response to reviewers' comments. However, no new experiments have been conducted to address questions raised by reviewers. The authors cited Allan Brain Atlas of parasagittally restricted receptor expression in the cerebellum. However, these are gene expression patterns in adult brain and definitely can not explain the observed phenotype of mutant animals. In general, results of this work are too descriptional and lack sufficient depth. These findings did not offer substantial new insights into the problem of how radial migration of Purkinje neurons is regulated during development.

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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.