Talking shop

The Frenchman has returned from his trek to Las Vegas, bearing many tales that I responded to by saying either "I can't believe you weren't arrested." or "I can't believe you WERE arrested." or "You're lucky you didn't die alone and naked in the desert." We have different ideas of what constitutes a vacation, the Frenchman and I.

So, we both sat down and met with PI New York today to discuss The Paper and Where it's Going and Holes. Every scientific paper ever written starts out with gaping holes. Many are easy to fill, like: where is your protein targeted to? Is your gene recessive or semi-dominant? Is this a loss or change of function mutation? etc. etc. Some are harder, like proving enzymatic activity. We have several large holes, most notable how we're relating our mutation to our initial avirulence effector. Since I am not a protein biologist nor a biochemist, I'm sort of out of my depth here.

However, to quote a famous boxing-glove and wrestling-mask wearing hero, I am "all up ons" the genetics of this project. Since I totally am one with with the subtle segregation nuances of my gene, I think I'm looking at a multi-allele segregation pattern, depending on the parental background of my F2s. This is both good and bad. The majority of my signaling mutants needed for epistasis are in the parental background with an allele that's interfering with my phenotype, so I'm not sure if my loss of phenotype is due to the mutation, or due to this gene X interference. But, on the plus side, I could map and clone this other gene, which is may be interfering with signal transduction. Ha ha ha I am on CRACK. Can you imagine generating a mapping population that is 1/16 of the F2s you plant?

So I've made a list of holes and things to plant and future experiments. I love to make lists. I find them satisfying. Never mind that I rarely accomplish things on my lists; it's just nice to know they're floating around.