1. Toxin: Marine Cone Snails By: Colin Coburn, Josh Goldfaden, and Brianna Williams http://www.bioconus.com/conus_victoriae_proboscis.JPG https://upload.wikimedia.org/wikipedia/commo ns/thumb/c/c0/Biohazard_symbol.svg/2000px- Biohazard_symbol.svg.png

2. 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

3. 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 that has been affected by toxin: the amino acid from the snail takes the place of the organism’s ligand and closes the channel. Cell’s normal function: the proper ligand from the organism regulates the ion content of the cells that lead to a cellular response. 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.

4. 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. 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. Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell Communication. In Biology (pp. 214-215). San Francisco: Pearson, Benjamin Cummings. https://www.mdc- berlin.de/34585359/de/research/research_team s/molecular_neurobiology/Forschung/T- toxins_illustration_for_HP_english.jpg

5. 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 paralysis 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 Without the presence of the ligand, ions are easily able to travel in and out of the cell (generate a response) because the normal messenger can attach to the ion channel. Campbell, N. A., & Reece, J. B. (2005). Chapter 11: Cell Communication. In Biology (pp. 212-213). San Francisco: Pearson, Benjamin Cummings.

6. 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.