Referee 2's review:

The present study by Larouche et al. describes structural abnormalities in the cerebella of mutants lacking the reelin receptors ApoER2 or VLDLR. The main finding is that different but partially overlapping subsets of Purkinje cells are abnormally localized in mutants lacking either ApoER2 or VLDLR. The authors arrive at this conclusion having studied these mutants with a variety of antibodies, including antibodies against calbindin, zebrin 2, and HSP 25. The study is of interest to researchers in the reelin field because it points to specific functions of the two reelin receptors ApoER2 and VLDLR. However, a couple of questions remain. The authors should address these points when they are going to revise their manuscript.

1. It would be nice to compare the expression patterns of ApoER2 and VLDLR in wild-type mice. Are there different populations of Purkinje cells expressing ApoER2 and VLDLR, respectively? It would be nice to see that the misplaced cells in ApoER2 mutants (i.e., mainly zebrin 2-negative Purkinje cells) do express ApoER2 in wild-type animals. Similarly, zebrin 2-positive cells, misplaced in VLDLR mutants, should be shown to express VLDLR in wild-type mice using combined immunohistochemical and in situ hybridization techniques or double in situ hybridization approaches.

2. Evidence from the literature suggests that glial differentiation may be affected in mutants with defects in the reelin pathway. Did the authors find some abnormalities in the arrangement of Bergmann glial cells?

3. As shown in Figure 1, the cerebellum is smaller in ApoER2 and VLDLR mutants, respectively. Is neurogenesis of Purkinje cells altered in VLDLR mutants or ApoER2 mutants?

4. By the same token, is there an increased apoptosis during cerebellar development in ApoER2 mutants or VLDLR mutants when compared to wild-type animals?

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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.