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In class, we discussed examples of “mutation” (in a general sense) via multiple mechanisms by which organisms, particularly pathogens, can gain new genetic material. (a) Now argue against this generalization: why are things like pathogenicity islands or transposons not the same as a mutation? ​

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Jean Keeling
Jean KeelingLv2
28 Sep 2019

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Related questions

1. Human Impact/Conservation

Okay...you’ve (hopefully) learned a lot about biology this semester. We have gone

from atoms, molecules, and cells through organisms and homeostasis, to populations,

communities, and ecosystems. Whew! Even though we started small, we still addressed

larger topics early on. Conversely, now that we have ended our intellectual journey with

ecosystems, we have circled back to talk about elements and molecules and cells. Over

the last couple of lectures, we have talked about human impact and conservation issues

that are challenging the global community.

1a. Of the human impact issues we talked about in class over the last week or two,

take one of them further.

• Clearly identify the issue you will be focusing on, and explain why

it is an important issue to address.

• Explain the biological principles addressed with this kind of

human impact.

• Examine what the natural order of things would be like without

humans being a part of the picture

• Next, re-insert humans into the picture. Identify the normal

biological properties that are impacted by this human activity,

and explain the impact disruption.

the issue would be deforestation.

In your answer, be sure to use specific biological examples and facts from your

notes and text. Use your new-found knowledge by applying it to show the

scientific basis behind one of the environmental crises our planet faces.

1b. Okay, now that the problem is identified and the nature of the disturbance is

explained, let’s talk solutions.

• How would you resolve this issue? What kind of societal things

can you install to bring about solution? Be practical in your

response. Identify stakeholders in the problem/solution, and the

(sometimes) competing interests

• Using what you know from this course (your notes and text),

explain how your above solution(s) resolve the underlying

biological problem(s).

In your answer, be sure to use specific biological examples and facts from your

notes and text. Use your new-found knowledge by applying it to show the

scientific basis behind a solution to one of the environmental crises our planet

faces.

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!

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