MCB 2050 Lecture Notes - Lecture 10: Cyclin E, P21, E2F

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sapphirecockroach400

23 Aug 2018

School

University of Guelph

Department

Molecular and Cellular Biology

Course

MCB 2050

Professor

ALL

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Document Summary

Genetic basis of cancer and the cell cycle. Process of tumour cell migration from on organ/tissue and establishment of new tumours in other organs/tissues. Non-metastatic tumours are benign: most tumours originate from epithelial tissues, because these cells are designed to proliferate (high levels of proliferation) Carcinoma: cancer of epithelial cells (makes up 90% of all cancers) Only when mutated will they induce cancer or fail to prevent its progression. Cell cycle checkpoints: there are checkpoints that are mechanisms for ensuring things are correct before progressing to next stage in cell cycle. G1/s checkpoint: regulates progression from g1 to synthesis stage, progression would need growth factor. Initially gf are required to begin this pathway but once cyclin e is produced at end, it is no longer dependent on gf. Inadequate or inappropriate apoptosis contributes to disease: many diseases associated with unregulated cell death.

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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!

QuestionGroup: #21 Gene expression 2

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Homework

The direct end result of gene expression is which of the following?

Amino acids

Translation

Proteins

Carbohydrates

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QuestionGroup: #22 Mutation

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Homework

Which of the following is the ways in which nucleotide mutations lead to altered proteins?

One nucleotide is substituted by another nucleotide, which can cause an early stop codon to be incorporated into the amino acid sequence resulting in a truncated protein.

One nucleotide is replaced by another nucleotide, which can change an amino acid in the protein sequence

Nucleotides are inserted into a nucleotide sequence causing a frameshift in the sequence.

All three choices may cause mutations.

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QuestionGroup: #23 Mutation 2

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Mutations are the result of which of the following?

Change in the normal nucleotide sequence in the DNA directly resulting in different carbohydrates

Change in the normal nucleotide sequence in the DNA directly resulting in different proteins

Change in the order of transfer RNA to messenger RNA so that the transfer RNA take over the role of Messenger RNA

Primarily an alteration in the sequence of nucleotides in the abnormal proteins

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QuestionGroup: #24 Cell division

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Homework

There are two major kinds of cell division. Which of the following plays a major role in promoting genetic diversity?

Meiosis since it causes the cells to make more daughter cells than mitosis

Mitosis since it causes the cells to duplicate and eventually have mutations

Meiosis since it causes the DNA sequences to be separated into new patterns in the daughter cells.

Mitosis since it essential for the ovaries in humans to separate and duplicate

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QuestionGroup: #25 Cancer

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Homework

Genes that slow down or stop the cell cycle are called...

Apoptotic genes

Oncogenes

Restriction genes

Tumor suppressor genes

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QuestionGroup: #26 Cancer2

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The common theme in the development of all cancers is...

Mutation

Evolution

Infection

Syncopation

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QuestionGroup: #27 Genetics

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Homework

Punnett's square is which of the following?

Example of all possible combinations of alleles

Example of all possible combinations of chromosomes

Example of only certain combination of alleles since some will not be expressed.

Example of all possible combinations of DNA

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QuestionGroup: #28 Embryo development

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Which of the following is the end of the cleavage phase?

A fetus

Formation of a blastocyst

Implantation to the lining of the uterus

Fewer number of cells

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QuestionGroup: #29 Development of organ system

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For organs to be differentiated, which of the following is the first step?

Stem cells trigger the development of differentiated cells

Tissues assemble into organ systems such as blood

Tissue specific genes in stem cells are triggered

Differentiated cells form tissues

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QuestionGroup: #30 Development and society

Assigned as

Homework

A pregnant mother ingests a chemical which her mother said would be great for the baby. When the baby was born, it had a large head and flippers for arms. What caused this phenotype?

The chemicals were teratogens which influenced oxidative phosphorylation causing the changes in the phenotype.

The chemicals influenced the expression of different stem cells.

There is no way to assume the chemicals caused the phenotype since we have no data on other mothers who took this medicine. It could have been purely by chance.

The chemicals were teratogens which caused the baby to show early signs of evolution.

MCB 2050 Lecture Notes - Lecture 10: Cyclin E, P21, E2F

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