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TOWSON / Biology / MBBB 309 / What is epistatic in genetics?

What is epistatic in genetics?

What is epistatic in genetics?

Description

School: Towson University
Department: Biology
Course: Genetics
Professor: Masters
Term: Spring 2016
Tags:
Cost: 25
Name: Bio 309 Genetics Week 12 Notes
Description: These notes cover material from 4/25 to 5/2.
Uploaded: 05/03/2016
8 Pages 37 Views 1 Unlocks
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Epistasis: is when the phenotype effect of a gene can be affected by another gene (or genes). Most traits have many epistatic interactions.We also discuss several other topics like What is an “open rate” in newspaper?

Don't forget about the age old question of When must one record revenue?

Pleiotropy is when a single gene can affect many traits

Don't forget about the age old question of Who founded the game theory?

Example: A single base change in the gene coding for hemoglobin can cause sickle-cell anemia with numerous phenotypic effects.

Most traits are actually determined by multiple loci such traits are referred to as polygenic.We also discuss several other topics like What are the common figures and patterns of masks in africa?

Don't forget about the age old question of What is a kinship system? who does it include? are all kin biologically related?

Per trait mutation rates one 0.1 and whole genome mutation rates are 1.0, therefore there cannot be a large number of genetically independent traits.

We also discuss several other topics like What are the president's enumerated powers?

The actual picture seems likely to result from multigenic effects, epistasis and pleiotropy.

  • In cancer cells, P53 has been enclosed at and doesn’t function
  • Study was done on 4 groups of people with lung cancer and that determined mutation on P53 gene. Groups were smokers, non smokers, drinkers, non drinkers

       

Armitage and Doll proposed a model in 1954 in which cancer was based on a need for a number of discrete and independent events.

So, why hasn’t evolution introduced more checks so that cancer requires even more mutations?

  • The longer you live, the more your cells replicate, the more likely you are to have cancer

Leukemia would require less discrete events/critical mutations than prostate cancer

  • If we were to cure all forms of cancer, the average lifespan would only increase by 2 years

  • Most people who die of cancer are relatively old- doesn’t decrease setness

  • Genetic variation in cancer, predisposition: mutational; decay of a robust genetic centered network

Introducing extra steps in cancer progression results in the accumulation of non-lethal mutations that increases genetic predisposition to cancer.

This predisposition will be unevenly distributed in the population

Where N=8, 85% of the risk will be concentrated in the most at risk 30% at the population

In actual data for breast cancer, 88% of cases are found in the 50% of the population that is most at risk

Mutations that would give you a predisposition for prostate, colon, breast, etc cancer wouldn’t be decreased through evolution because most people get it post reproductive age and it doens’t affect fitness

However, it is unlikely for a person to be born with a mutation that increases risk for leukemia because it decreases peto’s paradox.

  • There is little relationship between cancer rates and body size and longevity in animals

Potential Mechanism: for cancer resistance in elephants and comparative cellular response to DNA damage in humans.

  • Elephants have 20 functional copies of the p53 gene and lymphocytes show increased rates of apoptosis in response to DNA damage
  • Related species like hyraxes and manatees only have one copy of the p53 gene
  • Elephant cancer mortality is 5% (human cancer mortality is 11-25%

P53 responds to damage to DNA and causes the cell to undergo apoptosis

A cell without p53 i8 (1p53 copy instead of 2) is much less likely to undergo apoptosis

Mice were genetically engineered to have an extra p3 gene. They didn’t get cancer, but their lifespan was shorter because the stem cell die prematurely

Carcinomas are cancers that arise from epithelial tissue and one by for the most common type of cancer .

  • Why would epithelial cells be more likely to become cancerous than other types of cells?
  • Epithelial cells are constantly going through the cell cycle. The more DNA gets replicated, the more likely that mutation will occur.

  • Because epithelial cells are constantly going through the cell cycle, there may be fewer checkpoints on constant replication.

  • Epithelial cells are more likely to be exposed to environmental mutagens

Characteristics of Cancer Cells

  • Unregulated replication (loss of cell cycle control)
  • Loss of contact dependence M cell culture (formation of masses instead of a monolayer)
  • Disorganized cytoskeleton
  • Synthesis of unusual cell surface proteins
  • Aneuploidy (massive increase in mutation rates)
  • Altered oxidative metabolism

P53 actually does a number of things

  • Activates transcription of p21 which blocks progression through g1lb checkpoint
  • Activates transcription of gadd45, which blocks progression through

Reactivation of latent HIV by historic deacetylase inhibitors

  • The “ shock and kill” approach combines induction of latent HIV by HOAC inhibitors in combination with anti-resources therapy
  • Nota Bene: histones are used to control transposable element activity and the suppress integrated reisviruses.
  • DNA is mutilated globally, which causes a histone complex to bind and shutdown expression of HIV viruses
  • This is a bad thing for latent HIV. They want the virus to function while it is being treated with the anti-reversal therapy so they can kill it. They can’t kill latent HIV

The CD47 -Signal Regulatory Protein Alpha (SIRPA) interaction is therapeutic target for human solid tumors

  • CF47, a “ don’t eat me” signal for phagocytic cells, is expressed on the surface of all human solid tumor cells. Analysis of patient tumor and matched adjacent normal (non tumor) tissue reveals that CD 47 is overexpressed on cancer cells.

  • High CD47 levels are bad for cancer patients because they can survive attack from the immune system

  • This suggests cancer therapy card target CD47, leaving cancer cells with low CD47 to be eliminated by the immune system

In order for cancers to travel in the body, it has to survive travel through the bloodstream, which many don’t. They also have to figure out how to break through the basal lamina to reach the bloodstream.

Cells have to raise the mutation rate enough but not too much in order to become cancer cells

  • If you push the mutation rate of only cancel cells up, they will self destruct

Warburg’s Theory was that cancer started from irreversible changes to cellular respiration

  • Significant alterations were observed in cardiolipin content or composition in all types of tumors analyzed
  • Changes were closely associated with significant reductions in energy-generating activities.

Reactive oxidative species (ROS) cause damage to cardiolipin

This causes the release of cytochrome C

This induces apoptosis

This is a possible anti-cancer mechanism that causes destruction of cells when they become badly damaged by oxidation

Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progression

  • Tumor cells typically have altered metabolism and frequently segment glucose rather than utilize oxidative metabolism. They produce pyruvate from glucose and convert tht to lactate to regenerate NADH molecule cells need lactate dehydrogenase A (LDHA) to convert pyruvate to lactate

An inhibitor of LDGA (fxll) was shown to have efficacy in reducing tumor size. It works even better when used in combination with an inhibitor of NAD4 synthesis.

Cancer Genes

-Oncogenes are genes that when mutated, actively promote cancer Ex.ROS

-Tumor Suppressor genes are genes that  when mutated, fail to repress cancer. Typically, oncogenic transmission of tumor suppressor genes results in their inactivation. P53 is the typical tumor suppressor gene

Ras is an oncogene. It is inactive when found to GDP . If there is a certain extracellular signal, Ras drops the GDP and rises up a caTP. That activates the Ras protein and signals the cell to divide. Quickly after the GTP is degraded and Ras is inactive again.

In the mutated Ras, it is always bound to GTP and therefore always activated. This signals continuous cell division.

Proto-oncogenes are normal genes that can become oncogenes through a deletion or  permutation in coding sequence, gene amplification, or chromosome rearrangement (transposable element jumps, mutation in cos region, promoter or enhancer)

Expect less methylation in a proto-oncogene because overexpressed.

Expect more methylation on a tumor suppressor gene

Another mutation that could occur is if methylation on a transposable element is decreased and it jumps and activates a proto-oncogene.

Transmissible Dog cancer genome reveals that origin and history of an ancient cell lineage

  • CTVT first arose on a dog with low genome heterozygosity that may have lived about 11,000 years ago
  • The cancer spawned with this individual dispersed across continents about 500 years ago
  • Our results provide a genetic identikit of an ancient dog and demonstrate business of mammalian somatic cells to survive for millenia despite a massive mutation burden
  • The tumor originated from a group of dogs that was so inbred that when it jumped, the other dogs didn’t recognize it as foreign
  • 500 years ago, the tumor evolved so that it could jump to an unrelated dog and still not cause an immune response

Tasmanian Devils are very inbred. They are also aggressive and fight each other. When they fight, if one with the cancer bites one without the cancer, they can easily spread the cancer since they are so inbred and the immune system doesn;t reject it. The tumors are typically on their face.

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