Review for "Endodermal differentiation is reconstructed by coordination of two parallel signaling systems derived from the stele in roots"

Completed on 22 Nov 2017 by Jose R Dinneny . Sourced from

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Comments to author

We discussed this manuscript in our journal club yesterday and have the following comments to make:
The manuscript of Li and Yu et al., shows a lot of potential to gain better insights in systemic SHR function and CS formation. In order to fully understand the novel findings of this manuscript, it would be advisable to more appropriately reference the respective figures and supplemental figures in the main text.

Since the authors are mostly using estradiol inducible lines, it would be helpful to see the expression of the respective proteins upon induction to determine if the effects are a consequence of cell autonomous or non-autonomous signaling.

In figure 1a and b it remains unclear why the authors expressed pCASP1:CASP1-GFP in a 35S:SHR-GFP line. A second fluorophore would add to the clarity of the phenotype.

In figure 2 and 3: the expression pattern of the GFP fusion reporters would benefit from additional visual aids like cell file labels and arrowheads pointing to the phenotype.

In supplementary figure 4 the authors show that inducible MYB36 expression can induce CASP1-GFP expression in a shr-2 background. What remains unclear is the mislocalization of the CS. It was previously shown that SCR is still expressed in the endodermis of shr mutants. If SCR was involved in CS localization, it could still be functional in shr mutants. Analysis of a shr scr double mutant may clarify the interpretation.

In figure 3 B the authors suggest that SHR acts as a master regulator whereas MYB36 rather acts as intermediate hub. It remains unclear, however, why MYB36 activates gene expression so much stronger than SHR.

The findings of figure 4 are compelling. However, the authors claim that CIF1 and 2 are not regulated by SHR, because they cannot see any expression activation in SHR and MYB36 inducible lines. Have you also checked CIF1 and 2 expression in shr mutants?

Figure 5 D: How was the apoplastic transport of CIF1 and 2 shown?

(Supplementary) Figure 5: Would CIF2 treatment also be enough for CS formation outside of the endodermis? Could CIF2 lead to CS formation above the “restriction zone”?

The authors should more clearly define what aspects of SHR/MYB36 function have been described in previously published work and what findings the current manuscript describe.

Overall, the two major questions that are remaining are:
What is the role of SCR in CS localization?
What prevents the epidermis from CS formation? Is it only the promoter activity of the inducible transgenes used?

Best wishes,
The Dinneny Lab