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Wednesday August 30, 2006 week two Qs from gallagher et al
1). they found that the SHR protein transloctates itself throughout the
stele, and that pressumably, this occurs via plasmodesmata. I want to
ask, how would you conduct a test to show that it does so? I am not
certain if you would want to block out the plasmodesmata, but could you
do a protein fusion with SHT that would somehow be big enough to not
fit (in other words, size exclusion).
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1) If a point mutation decreases nuclear localization and movement both then the why state that if SHR is in the nucleus that it does not move between cells since it must need the nuclear localization sequence for both?
2) If SHR interacts with a cytoplasmic trafficking molecule would the exportin be needed to make sure that the SHR moved to the endodermis since the protein is presumably made the cytoplasm to begin with.
3) Could SHR use the nuclear localization sequence to move to the ER and then be transported between cells in this fashion, instead of having a specific nuclear exportin which is rare?
4) This would suggest that another protein is moving between the cells to trap the SHR in the nucleus of the next cell layer, what evidence is there for large protein complexes to move between cell layers?
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1) Why the big deal over no movement when SCR is dragged into the nucleus by the GFP-nls? Isn't it obvious that something powerfully drawn to the nucleus isn't going to leave the cell? Are there situations in which something with a strong nls would still be exported?
2) Why does proper folding of proteins affect GFP fluorescence? And why does the scr-5 mutation induce STRONGER fluorescence?
3) What is NetPhos?
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What is/how do you get an En element?
What exactly is partial reversion process?
What is non-cell autonomous?
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1) "presence of SHR in these adjacent tissues correlates with expression
of a related gene, SCARECROW" - Does this mean that SHR is a transcription
factor for SCR?
2) Does 'nontargeted movement' mean that the protein simply diffuses
across the cell wall?
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1) Regarding the fact that the SHR-nlsGFP was not detected in the root
cells, how does the nuclear localized GFP not affect the SHR stability?
2) Could the authors do some sort of plant assay in the SHRT>I mutant and
look for disruptions in other known proteins used in trafficking?
3) Could they use a chemical that allows diffusion of proteins across
intercellular membranes to also verify that the SHR protein can move when
stimulated?