Today''s Page Hits: 24
This page validates as XHTML 1.0, and will look much better in a browser that supports web standards, but it is accessible to any browser or Internet device. It was created using techniques detailed at glish.com/css/.
Wednesday September 06, 2006 questions for sept 10th
1) On page 744, the authors discuss the target validation for 4 out of the eight candidates. They describe expression patterns for SCR, MGP, NUC, but their is no evidence for TRI, is there?
2) What type of mutations are shr-2 and shr-4 - missense, nonsense, etc.?
3) On page 746, the authors discuss the meta-analysis findings for genes indirectly related to SHR. For example, they said they identified 56 genes for statistically significant putative transcription factors either repressed or activated by the SHR pathway in the root. Much of the time there could be redundant genes observed by this type of analysis - how could they detect the redundant candidates before the sequence is known or is the sequence known already (this part unclear to me)?
-----------
1. How does a meta analysis evaluate gene expression?
2. In the stele marker experiment what is the phenotype
and explanation for almost half of the results not
being an expansion of the expression domain?
3.How does CHIP-QRT-PCR work?
---------------------
Although it does make sense, I am still not sure how the authors
concluded that the uneven GFP expression was due to assymetric cell
division in figure 2J? Could it not been random expression or uneven
presence of Dex in their media? They did mention that they were able to
see only a few assymetric divisions. My second question is about this
whole meta-analysis. Is this just a fancy statistical way to be more
stringent on the genes they select, because they do mention it as been
never been used before, so I am not sure if there's more to this or
not.
--------------
1) How can they determine that the expression of SHR itself is causing the
changes in hormones and it is not just the change in the Stele that is
causing transport changes?
2) Why is the assumption that the direct over expression study the basis
for the best comparison? It could be that the knock out study shows the
more direct interactions by what changes, so could they not have used each
of the three studies as the base studies.
3) I do not like their assumption that the proteins that regulate hormone
production could only be affecting the hormone production. I would argue
that we need to see data for the hormone changes (ie staining or
quanitation) before I would accept the direct affect of SHR on hormones
that they are noting in their model.