BIO 201 Lecture Notes - Lecture 4: Adaptive Immune System, Mutation Rate, Genetic Drift

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silverbutterfly439

29 Jun 2016

School

Stony Brook University

Department

Biology

Course

BIO 201

Professor

John Trueand Ross Nehm

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Document Summary

If they cause bad effects (deleterious), individuals carrying them usually die or have low survival and/or reproduction. Deleterious mutations are usually quickly eliminated from the population. When we sample a population, we don"t find them. Unless they are recessive then they may increase to a low frequency by chance (or because in a past environment, they were advantageous. If they have no effect (neutral) or have beneficial effects, they may survive but still usually lost by genetic drift. The battle against flue is a battle against the effects of evolution. Influenza viruses have an rna genome encoding 11 proteins. Many different strains exist in the human population any given year. Only a few survive to yield infectious viruses the next year. Strains with the most changes in surface proteins tend to be the best survivors. By studying many strains over many years, researchers now know which amino acid positions in the surface proteins tend to evolve quickly.

Related Questions

Recently I have found myself in a discussion with a guy thatisn't a creationist, but denies evolution. He cites several studiesthat show problems like this one, but I do not have the knowledgeto refute it properly. Whats the problem with the following:

One problem is that population genetics shows us evolutiondestroys functional sequences much faster than it creates them inany large-genome animal with low reproductive rates, becausedeleterious mutations arrive faster than selection can remove them.This would include just about all mammals, reptiles, and birds--anyof our would-be ancestors over the last 300m years.

Specifically, humans get 60 to 160 mutations per generation,10-20+% of our genome is sensitive to substitution, and this givesus 6-32 deleterious mutations per offspring (most slight). Evenwith the low estimate of 6, every child is less fit than theirparents and natural (or even artificial) selection can only choosethe least degenerate each generation. For every generation where amutation can be selected, random mutations destroy 5-32+ previouslyselected. Beneficial mutations like lactose tolerance (a jammedswitch) take 1000s of years to appear and fixate.

If you know the genome size, mutation rate, and reproductiverate, you can calculate at what rate deleterious mutations arrivefaster than they can be removed:

"It has been estimated that there are as many as 100 newmutations in the genome of each individual human. If even a smallfraction of these mutations are deleterious and removed byselection, it is difficult to explain how human populations couldhave survived. If the effects of mutations act in a multiplicativemanner, the proportion of individuals that become selectivelyeliminated from the population (proportion of `genetic deaths') is1-e^-U, where U is the deleterious mutation rate per diploid, so ahigh rate of deleterious mutation (U>>1) is paradoxical in aspecies with a low reproductive rate." High genomic deleteriousmutation rates in hominids, (Nature, 1999)

They worry about a deleterious rate of U much greater than 1 asbeing prohibitively high and we're talking about it being 6-32+,since we now know the functional genome is much larger than wethought it was in 1999. Taking their Poisson probabilitydistribution and using U=6, that means 1-e^-6 = 99.752% of thepopulation will have to be selected away each generation for onelucky enough to have no deleterious mutations. For two to surviveand maintain constant population size that would require on average806 offspring per female--impossible for most mammals, birds, andreptiles. Actually much more since natural selection is notomnisciently efficient.

1. Humans and chimpanzees share several polymorphic loci. Which is the LEAST plausible explanation for this fact?

A. Balancing selection has maintained polymorphism in both species

B. Incomplete lineage sorting left polymorphic loci and those have persisted since the speciation event.

C. Interbreeding has allowed introgression of alleles at theses loci in both directions.

D. Genetic variation provided by the polymorphic alleles enhances resistance to pathogens.

2. According to the social brain hypothesis, we should expect primates living in larger social groups to have:

A. Larger brains, specifically, a neocortex of relatively larger size

B. Lager incisors and canines, to defend against more social competitors

C. Smaller brains, because many individuals can work together to solve problems

D. Great variation in brain and neocortex size, with the dominant individuals having the largest

3. You extract DNA from human bones in an ancient village buried by volcanic ash. You discover that there is an extremely high frequency of the LCT allele for lactase persistence. What might you reasonably conclude about the population?

A. This population is likely the source of the high frequency of the LCT gene in Northern Europe

B. The village could not be more than 4,500 years old

C. The members of this population likely used domesticated livestock for their milk

D. villagers had a diet rich in wheat or another domesticated crop

4. Why do populations father from Africa have more deleterious mutations in their genome?

A. Repeated bottlenecks and founder effects made drift more intense more often

B. Populations farther from Africa have been exposed to more mutagens in the environment

C. As people migrated over the globe they interbred with Neanderthals and Denisovans

D. The populations are younger, so purifying selection has not had time to purge delirious mutations from the populations.

yelloweel732

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!

BIO 201 Lecture Notes - Lecture 4: Adaptive Immune System, Mutation Rate, Genetic Drift

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