Questions+3-1-13


 * Zhao 2001**

Do you think screening an activation-tagged mutant population was the best strategy? Who or why not? Can you think of a situation in which this wouldn’t work?

What led the authors to test YUCCA activity on tryptamine?


 * Won 2011, Mashiguchi 2011**

What led these authors to doubt tryptamine was the substrate for YUCCA? Some of this may be in the introduction…

Why are higher order //yucca// loss-of-function mutants necessary to see low auxin phenotypes?

What is the evidence YUCCA converts IPyA to IAA? Is this evidence stronger than the evidence YUCCA converts tryptamine to N-hydroxy-tryptamine?

What level of evidence should be necessary to change an established model? Should the bar be set higher for altering a model than for first establishing one? How do scientists come up with these models?

Do you think Trp-to-IPyA or IPyA-to-IAA conversion is the limiting step in this pathway? Why?