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Regarding comments of Dr. Duester

Posted by sampleasure on 04 Apr 2013 at 19:35 GMT

I would draw the interested reader's attention to the previous comments regarding the study that Dr. Duester refers to here - also published in Plos One for some context regarding this issue. We stand by the findings in the current study and those in Siegenthaler et al., 2009 and do not feel that Chalzi et al is definitive in the way that Dr. Duester would like to present it here. As is clear from the comment thread at the link below there are a number of issues we raised that Dr. Duester chose not to address.

http://www.plosbiology.or...

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RE: Regarding comments of Dr. Duester

duester replied to sampleasure on 05 Apr 2013 at 11:33 GMT

I find it disturbing that Dr. Pleasure thinks it is OK to simply not reference Chatzi et al. 2011 (PLoS Biology) in his PLoS ONE paper. Is he afraid of the findings in that paper? I have made another post for Chatzi et al. 2011 (PLoS Biology) to address Dr. Pleasure's concerns of 2 years ago.

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RE: RE: Regarding comments of Dr. Duester

sampleasure replied to duester on 05 Apr 2013 at 18:39 GMT

I will not respond to ad hominem attacks, particularly from someone I've never met...

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RE: RE: RE: Regarding comments of Dr. Duester

duester replied to sampleasure on 06 Apr 2013 at 09:37 GMT

But you are responding to the Comments for my PLoS Biology (2011) paper, so here I will add my last response to you from that paper to help readers evaluate your PLoS ONE paper. From your last comments on my PLoS Biology (2011) paper, you admit that we have demonstrated that our Raldh2-/- embryos have indeed lost the RA generated in the meninges that diffuses to the cortex. However, you appear to be changing the goal posts by saying that there might be another way for the cortex to obtain RA. This is in contrast to your Siegenthaler et al. 2009 Cell paper that proposed the meningeal diffusion model based on expression of both Rdh10 and Raldh2 in the meninges (but a lack of these enzymes in the cortex) thus allowing RA to enter the radial glial endfeet. If you think there is a compensatory mechanism for providing RA to the cortex then it is up to you to demonstrate this and provide data on what enzymes are required. Only then can you claim that RA acts in the forebrain to control cortical expansion. However, in this case your mechanism of meningeal RA entering through the endfeet (which is the title of your Cell paper) is incorrect.

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RE: RE: RE: RE: Regarding comments of Dr. Duester

sampleasure replied to duester on 06 Apr 2013 at 14:34 GMT

Again, I do not accept your formulation of my statements. I point out difficulties in the interpretation of the RALDH2 mutant mice. It is up to you to address the potential ways that those mice may have developmental compensation. The simple fact is that in the Chatzi et al paper the analysis of whether there is RA in the cortex and where it comes from relies ENTIRELY on a bioassay with major limitations. Our study (Siegenthaler et al) which appeared two years earlier uses MANY lines of evidence to propose what we believe to the model of how RA affects cortical expansion and development.

I have pointed this out now time and time again in the comments on the other paper.

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