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- Aug 27, 2007
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Hi, I've been doing work on C. elegans in a neurological genetics screen. One of the phenotypes of my primary "prized" mutation is defective axon guidance. The commissures on my works are quite abnormal.
I have several abnormal phenotypes to compare the axon guidance defects on, but I have no reference with which to compare; ultimately I don't know if its logical or reasonable to tie defective axon guidance to my various phenotypes.
So I was wondering if anyone knew how most axon guidance defects manifested (of even if there was a textbook manifestation of axon guidance defects).
Specifically, my worms experience severe paralysis, abnormal sensitivity to acetylcholinesterase inhibitors, and an inability to lay eggs. I believe these phenotypes are due to excessively long and winding commissures, but how they fail to signal the body wall muscles I have no clue.
I have several abnormal phenotypes to compare the axon guidance defects on, but I have no reference with which to compare; ultimately I don't know if its logical or reasonable to tie defective axon guidance to my various phenotypes.
So I was wondering if anyone knew how most axon guidance defects manifested (of even if there was a textbook manifestation of axon guidance defects).
Specifically, my worms experience severe paralysis, abnormal sensitivity to acetylcholinesterase inhibitors, and an inability to lay eggs. I believe these phenotypes are due to excessively long and winding commissures, but how they fail to signal the body wall muscles I have no clue.