Rough-skinned newt

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Rough-skinned Newt

Conservation status

Least Concern

Scientific classification

Kingdom:	Animalia
Phylum:	Chordata
Class:	Amphibia
Order:	Caudata
Family:	Salamandridae
Genus:	Taricha
Species:	T. granulosa

Binomial name

Taricha granulosa

The rough-skinned newt (Taricha granulosa) is a North American newt known for its strong poison. They are available in some places as pets, sometimes with names "Oregon newt" or "orange-bellied newt." However the "Oregon newt" is more than likely a newt from California that looks similar. Oregon does not allow the commercial sales of these newts.

1 Subspecies
2 Toxin
3 Toxin Resistance and Predation
4 Location
5 See also
6 References

[edit] Subspecies

T. granulosa is divided into two subspecies. Both have rough or granular skin, except for breeding males, which additionally swollen vents and cornified toe pads.

The rough-skinned newt (T. g. granulosa) is light brown to brownish-black above with an orange or yellow belly. In some populations, the back has dark blotches. They are between 13 to 22 cm long.
The Crater Lake newt or Mazama newt (T. g. mazamae) is darker above and brighter below than T. g. granulosa and may also have dark blotches below. The validity of this subspecies, which is exclusive to the region of Crater Lake, Oregon, is disputed by some researchers because the newts on Gravina Island, Alaska, are very similar.

[edit] Toxin

Many newts produce toxins to avoid predation, but the toxins of the genus Taricha are particularly potent. The Rough-skinned Newt produces tetrodotoxin, which in this species is sometimes called tarichatoxin. One thirtieth of the toxin present in the skin of an average adult rough-skinned newt is sufficient to kill a healthy adult human. The toxin is generally only toxic if the newt is ingested, although there are reports that some individuals experience skin irritation after dermal contact.

[edit] Toxin Resistance and Predation

Throughout much of the newt’s range, the common garter snake (” Thamnophis sirtalis”) has been observed to exhibit resistance to the tetrodotoxin produced in its skin. The toxin binds to sodium channels in nerve cells and interferes with the normal flow of sodium ions in and out of the cell. This has the effect of inducing paralysis and death. The toxin binds to a tube shaped protein that acts as a sodium channel in the snakes nerve cells, however researchers have identified genetic mutations in several snake populations that alter the protein in such a way as to hamper or prevent binding of the toxin. In each of these populations, the snakes exhibit resistance to the toxin and successfully prey upon the newts. The relationship between the rough-skinned newt and the common garter snake is an example of co-evolution. The mutations in the snake’s genes that conferred resistance to the toxin have resulted in a selective pressure that favors newts which produce more potent levels of toxin. Increases in newt toxicity then apply a selective pressure favoring snakes with mutations conferring even greater resistance. This cycle of a predator and prey evolving to one another is sometimes termed an evolutionary arms race and has resulted in the newts producing levels of toxin far in excess of what is needed to kill any other conceivable predator. Today, toxin resistant garter snakes are the only animals that can eat a T. granulosa newt and survive.

[edit] Location

Rough-skinned Newt, Fairfield Osborn Preserve.

Habitats of rough-skinned newts are found throughout the west coast of the US. They are uncommon east of the Cascade Mountains though occasionally found (and considered exotic, and possibly artificially introduced) as far as Montana. The southern range extends to Santa Cruz, California and as far north as Alaska. ^[1]

[edit] See also

[edit] References

Hammerson (2004). Taricha granulosa. 2006 IUCN Red List of Threatened Species. IUCN 2006. Retrieved on 12 May 2006.
Taricha granulosa: Rough-skinned Newt. Caudata Culture. Retrieved on 2006-07-26.

Geffeney, Shana L., et. al. “Evolutionary diversification of TTX-resistant sodium channels in a predatorÂ-prey interaction”. Nature 434 (2005): 759–763.