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23 Nov 2019

Consider the figure below. During which year does the 1 year old age class make up the highest percentage of the population of Tasmanian devils on the Freycinet Peninsula?

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Related questions

The Tasmanian devil, a marsupial indigenous to the island of Tasmania (and formerly mainland Australia as well), experienced a population bottleneck in the late 1800s when farmers did their best to eradicate it. After it became a protected species, the population rebounded, but it is now experiencing a health crisis putting it at risk for disappearing again. Many current Tasmanian devil populations are plagued by a type of cancer called devil facial tumor disease, which occurs inside individual animals’ mouths. Afflicted Tasmanian devils can actually pass their cancer cells from one animal to another during mating rituals that include vicious biting around the mouth. Unlike the immune systems of other species, including humans, the Tasmanian devil’s immune system does not reject the passed cells as foreign or nonself (as we reject a liver transplant from an unmatched donor), but accepts them as if they were their own cells. Why would a population bottleneck result in the inability of one devil’s immune system to recognize another devil’s cells as foreign? ANSWERS WITHIN ONE SENTENCE:

Tasmanian devils (Sarcophilus harrisii), the world’s largest carnivorous marsupials, are facing extinction. Not from hunting, or habitat loss, but from within; a transmissible cancerous derivative of Schwann cells, responsible for devil facial tumour disease (DFTD). First seen in 1996, the disease has spread widely though the population, and is now estimated to be present in 80% of the population. With the grim prognosis of ~100% mortality in 12-18 months, animals that once went through multiple breeding cycles are now lucky to reproduce once before death, resulting in a 70% decline in their population over the past decade. The cancer is transmitted by biting (a common ritual used by these animals to establish and maintain social position), with cancer cells from one animal (the biter) being implanted in the wound inflicted on the other animal. Equally common in both sexes, the disease itself is more prevalent in animals higher on the social scale, presumably reflecting higher levels of social interaction (biting). The cancer is usually first evident as facial tumors, from which metastasis to cervical lymph nodes occurs, often followed by dissemination to other organ systems. Cause of death is by organ failure or by malnutrition in those with facial tumors large enough to prevent feeding. Based on what we have covered regarding the Major Histocompatibility Complex, you would expect the passage of a cancer from one individual to another* to be a rare event (to see just how rare, read the accompanying popular press piece from the New York Times). Here are some things that you already know: *Yes, some viruses can cause cancer (example: Hepatitis B virus and liver cancer), and you can transmit a virus from one individual to another; but that is not the same thing as passing the cancer itself. v Almost all nucleated cells express high levels of class I MHC proteins on their surface. v Class I MHC proteins collect peptides produced from endogenous proteins and display them at the cell surface. v Different Class I MHC proteins bind and display different peptides. v Developing cytotoxic T-cells that recognize self-antigens are eliminated. v Mature cytotoxic T-cells conduct surveillance by scanning the peptides displayed by class I MHC proteins. v Mature cytotoxic T-cells that recognize an antigen on a cell will kill that cell (recall that cytotoxic T cell activity is important in rejection of tissue transplants).

Before the questions:
v Tasmanian Devils are not immunosuppressed.
v Tasmanian Devil cytotoxic T-cells are not broken, they can kill cells.
So neither of those should be part of your answers.
This is an ongoing research topic with large gaps in our knowledge; we really don’t fully understand how this works
and so there is no “correct” answer. Your job is to provide a logical argument, with some research and details to
support your contention. Note that in questions 1 & 2 class I MHC should be part of your answer, but not in
question 3.

Questions:
1.) Acquiring DFTD is basically like receiving a transplant that is not rejected. How can that be? Suggest a possible
way this could occur. Be sure to explain why you think this would work, and then explain how you would test
that model to determine if it were correct. (10 point question).
2.) Canine Transmissible Venereal Tumor (CTVT) is the other know transmissible cancer in mammals. Unlike
DFTD, CTVT does not usually result in death. Do a little research on this disease and summarize how it is
different from DFTD. Provide an explanation as to why one is lethal and the other is generally not. (10 point
question).
3.) Recently, researchers at Washington State University determined that some Tasmanian devils had developed
resistance to this cancer. By scanning partial genome sequences of resistant and susceptible animals (a
complete devil genome has yet to be assembled) they identified a set of genes where mutations appeared to
enhance resistance. Speculate as to the function of the proteins these genes encode, and explain why that
might provide for resistance (note: they were NOT MHC genes).

Mainly need guidance/ideas for #1's 1 and 3!

Consider an age-structured population with a stable age distribution. On average, newborn females have three female offspring in the course of a lifetime, and the middle female offspring is born when the mother is 10 years old.

(a) write the equation for the actual instantaneous per capita ggrowth rate for this population. Except for the symbol representing this rate, the equation must have only numbers.

(b) Write the equation for solving how long will it take this population to double (you don't have to find how long it takes, just set up the equation.)

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