Despite a century of research, memory encoding in the brain has remained mysterious. Neuronal synaptic connection strengths are involved, but synaptic components are short-lived while memories last lifetimes. This suggests synaptic information is encoded and hard-wired at a deeper, finer-grained molecular scale.
In an article in the March 8 issue of the journal PLoS Computational Biology, physicists Travis Craddock and Jack Tuszynski of the University of Alberta, and anesthesiologist Stuart Hameroff of the University of Arizona demonstrate a plausible mechanism for encoding synaptic memory in microtubules, major components of the structural cytoskeleton within neurons.
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Only have the time these days to share the abstracts of studies whose data support the hypothesis of FLE. Check this one out:
SNARE protein-driven secretion of neurotransmitters from synaptic vesicles is at the center of neuronal communication. In the absence of the cytosolic protein Munc18-1, synaptic secretion comes to a halt.
So why did I bring up the teneurins? Let’s consider the abstract of a paper that was published a few weeks ago :
Teneurins are type II transmembrane proteins expressed during pattern formation and neurogenesis with an intracellular domain that can be transported to the nucleus and an extracellular domain that can be shed into the extracellular milieu.
In other words, we have a protein that connect the nucleus to the environment outside the cell.
In Drosophila melanogaster, Caenorhabditis elegans and mouse the knockdown or knockout of teneurin expression can lead to abnormal patterning, defasciculation and abnormal pathfinding of neurites, and the disruption of basement membranes.
In other words, this is protein that plays an important role in the formation of brains and nerves. The fact that is carries out the same basic functions in worms, insects, and animals strongly suggests its role in nervous system is quite ancient and may have coincided with the emergence of the nervous system itself. So when did the tenurins arise?
According to Wikipedia,
Teneurins are transmembrane proteins. The name refers to “ten-a” (from “tenascin-like protein, accessory”) and “neurons”, the primary site of teneurin expression.
Teneurins are highly conserved between Drosophila, C. elegans and vertebrates. In each species they are expressed by a subset of neurons as well as at sites of pattern formation and morphogenesis. In Drosophila, a teneurin known as ten-m or Odz is a pair-rule gene, and its expression is required for normal development. The knockdown of teneurin (ten-1) expression in C. elegans with RNAi leads to abnormal neuronal pathfinding and abnormal development of the gonads.
And according to this article,
Teneurins are a unique family of transmembrane proteins conserved from C. elegans and D. melanogaster to mammals. In vertebrates there are four paralogs (teneurin-1 to -4), all of which are expressed prominently in the developing central nervous system.
So why mention these proteins?
Here is something that is pretty neat:
The size and shape of the human cerebral cortex, an evolutionary marvel responsible for everything from Shakespeare’s poetry to the atomic bomb, are largely influenced by mutations in a single gene, according to a team of researchers led by the Yale School of Medicine and three other universities.
The researchers found that mutations in the same gene, centrosomal NDE1, which is involved in cell division, were responsible for the deformity.
“The degree of reduction in the size of the cerebral cortex and the effects on brain morphology suggest this gene plays a key role in the evolution of the human brain,” said Murat Gunel, co-senior author of the paper and the Nixdorff-German Professor of Neurosurgery and professor of genetics and neurobiology at Yale.
“These findings demonstrate how single molecules have influenced the expansion of the human cerebral cortex in the last five million years,” Gunel said.
So here is a gene, Nde1, that has played a key role in the enlargement of the brain during human evolution. As the article notes, Nde1 is part of the centrosome, an organelle that functions to organize the microtubules throughout the cell. The function of Nde1 is not well characterized, but it is known to play a role in mitosis and neuron migration. So it makes sense that a crippled version of Nde1 might exhibit deficient levels of cell division and neuron migration, explaining the small brained phenotype.
So when did Nde1 arise?
I’ve been wanting to comment on this article by Mattick and Mehler, but have just been too busy. Luckily, I just ran across a web article that borrows heavily from M&M’s article. I would encourage you to read the whole thing (if you can’t get your hands on M&M’s article, that is). Here are some excerpts:
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Tagged alu, brain