Ed Chapman, professor of Neuroscience and HHMI investigator, and colleagues recently published in Nature Communications, Vol. 10, Article number: 3532 (2019), their work on synaptotagmin 17 (syt-17).
Synaptotagmins (syt) are generally thought to regulate exocytosis at the plasma membrane. Despite intense interest, only a minority of syt isoforms have been assigned any specific function. Using mice whose syt-17 gene was silenced, they discovered that halting production of synaptotagmin 17 (syt-17) blocked growth of axons. When mice cells were programmed to make more syt-17, axon growth accelerated.
A wide range of neurological conditions could benefit from the growth of axons, including spinal cord injuries and some neurodegenerative diseases.
“It’s a bit of a simplification,” says Chapman, “but basically, you can’t build without supplies, and one of the ways that neurons are able to build such long, complicated axons is through syt-17 speeding up the production line.”
For more information, click here: https://news.wisc.edu/single-protein-plays-important-dual-shipping-role-in-the-brain/