1.Does this divergence actually equate to speciation though? That is, are C. molestus and C. pipiens different species, or are they just different populations of the same species living in different locations?

2. What could Byrne and Nichols have done differently to strengthen their argument?

3. Why is it important for scientists to continually reexamine ideas and conclusions?

4. What do you think the next steps should be?

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Jarrod RobelLv2

1 Jul 2018

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Tasmanian devils (Sarcophilus harrisii), the worldâs 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 donât fully understand how this works
and so there is no âcorrectâ 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!