Doug- too much stuff to put into an actual calculation, but I doubt we have complete knowledge, given how little we understand epigentics (iRNA, 22URNAs, and other micro RNAs), synaptic transcription, cytoskeletal transport, microglial roles, the enteric nervous system, native neuro-regeneration, and low and behold, neurotransmitters themselves. The 3rd edition of Kandel I was taught out of as an undergrad said nothing of orexins, histamine, the other roles of meletonin beyond the pineal gland, or the functions of the multifarious set of cannibinoid receptors, yet we now know (a short 2 years later) that all of these transmitters seem to play critical roles. Now, not being an elegans gal, I don’t know if it has much simpler neurotransmission than we do. I would venture to guess it is simpler, but not extraordinarily so, and probably much more affected by simple epigenetic mechanisms like RNA interference. In C. elegans, iRNA messages are rapidly amplified, quickly shutting off the target gene in all of its cells (mammals have not been observed to amplify). Now, here’s the kicker- it gets into the germ cells too! So offspring will also produce iRNAs and shut off genes! Now, due to amplification error, iRNAs are eventually lost if the worms are bred long enough, but Craig Mellow is now exploring the hypothesis that amplified iRNAs can be eventually permenantly disable (viral) DNA that’s been incorporated into the C. elegans genome, either by more permenant epigenetic modification (methylation or coiling), or by splicing it out… Sorry for the MoBio lecture, but DUDE! This stuff is supercool!!!
Doug- too much stuff to put into an actual calculation, but I doubt we have complete knowledge, given how little we understand epigentics (iRNA, 22URNAs, and other micro RNAs), synaptic transcription, cytoskeletal transport, microglial roles, the enteric nervous system, native neuro-regeneration, and low and behold, neurotransmitters themselves. The 3rd edition of Kandel I was taught out of as an undergrad said nothing of orexins, histamine, the other roles of meletonin beyond the pineal gland, or the functions of the multifarious set of cannibinoid receptors, yet we now know (a short 2 years later) that all of these transmitters seem to play critical roles. Now, not being an elegans gal, I don’t know if it has much simpler neurotransmission than we do. I would venture to guess it is simpler, but not extraordinarily so, and probably much more affected by simple epigenetic mechanisms like RNA interference. In C. elegans, iRNA messages are rapidly amplified, quickly shutting off the target gene in all of its cells (mammals have not been observed to amplify). Now, here’s the kicker- it gets into the germ cells too! So offspring will also produce iRNAs and shut off genes! Now, due to amplification error, iRNAs are eventually lost if the worms are bred long enough, but Craig Mellow is now exploring the hypothesis that amplified iRNAs can be eventually permenantly disable (viral) DNA that’s been incorporated into the C. elegans genome, either by more permenant epigenetic modification (methylation or coiling), or by splicing it out… Sorry for the MoBio lecture, but DUDE! This stuff is supercool!!!