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Transcript
Toxin: Marine Cone
Snails
https://upload.wikimedia.org/wikipedia/commo
ns/thumb/c/c0/Biohazard_symbol.svg/2000pxBiohazard_symbol.svg.png
http://www.bioconus.com/conus_victoriae_proboscis.JPG
By: Colin Coburn, Josh Goldfaden, and Brianna Williams
Explanation of the Entity

The marine cone snail is a large snail that lives in many coral reefs. The snail
normally grows to be about 6 inches in size and is decorated with a white and
brown patterned shell. The snail has a toxin that can paralyze its prey
instantly. It uses its proboscis with a harpoon at the end, shoots its prey, and
injects it with the poison which causes the prey to be paralyzed. The snail
proceeds to eat its prey.
http://slappedham.com/wp-content/uploads/2014/06/Cone-snail.jpg
http://www.asnailsodyssey.com/IMAGES/WHELK/ArcherdShellCollection.jpg
Cellular Signaling of the Marine Cone
Snail

When poisoning its victims, Marine Cone Snails release toxins that are made
of various chemicals, specifically, amino acids. These amino acids act as
ligands that usually binds to the ion channels (transmembrane) of the victim’s
cells. The toxins from the snail close the channels and inhibit the diffusion of
ligands used in cellular communication within the victim. Normally, the ion
channels would be opened by the proper ligand, and ions would trigger the
response of certain functions within the cell.
Cell’s normal
function: the proper
ligand from the
organism regulates
the ion content of
the cells that lead to
a cellular response.
Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell
Communication. In Biology (pp. 212-213). San Francisco:
Pearson, Benjamin Cummings.
https://infogr.am/the-toxin-of-the-marine-cone-snail
Cell that has been
affected by toxin: the
amino acid from the
snail takes the place of
the organism’s ligand
and closes the channel.
Cellular Transduction of the Marine Cone
Snail

When a toxin is added to a normal ion channel, which is supposed to be open,
it blocks it/shuts it. This inhibits the process of transduction because the
receptor cannot send a signal if the ligand isn't received by the receptor,
which is blocked by the toxin. Therefore, no signal was ever received, and
transduction was never carried out.
https://www.mdcberlin.de/34585359/de/research/research_team
s/molecular_neurobiology/Forschung/Ttoxins_illustration_for_HP_english.jpg
Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell
Communication. In Biology (pp. 214-215). San Francisco:
Pearson, Benjamin Cummings.
Normally after a ligand bonds
to a receptor, that receptor
releases enzymes which then
help release secondary
messengers. Those secondary
messengers trigger the cell’s
response.
Cellular Response of the Marine Cone
Snail

With the toxin closing the ion channel, there is no way for the cell to receive
a message let alone go under transduction; therefore, no response in the
victim’s cell-the cells began to shut down due to their inability to carry out
communication to go against the toxin. In the end, the victim suffers from
Without the presence of the ligand, ions
paralysis
are easily able to travel in and out of
the cell (generate a response) because
the normal messenger can attach to the
ion channel.
With the presence of
the toxin (red) ion
channels in the
nervous system are
closed.
https://infogr.am/the-toxin-of-the-marine-cone-snail
Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell
Communication. In Biology (pp. 212-213). San Francisco:
Pearson, Benjamin Cummings.
Literature Sources

Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell Communication. In
Biology (pp. 212-213). San Francisco: Pearson, Benjamin Cummings.

Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell Communication. In
Biology (pp. 214-215). San Francisco: Pearson, Benjamin Cummings.

F. (n.d.). The Toxin of the Marine Cone Snail. Retrieved November 8, 2015,
from https://infogr.am/the-toxin-of-the-marine-cone-snail

"Geographic Cone Snails, Geographic Cone Snail Pictures, Geographic Cone
Snail Facts - National Geographic." National Geographic. N.p., n.d. Web. 09
Nov. 2015.