sources of variationagents of change mutationn.s. recombinationdrift - crossing overmigration -...

Sources of Variation Agents of Change

Mutation N.S.

Recombination Drift

- crossing over Migration

- independent assortment Mutation

Non-random Mating

VARIATION

So, if NO AGENTS are acting on a population, then it will be in equilibrium and WON'T change.

Modern Evolutionary Biology I. Population GeneticsA. OverviewB. The Genetic Structure of a PopulationC. The Hardy-Weinberg Equilibrium Model 3. Utility: - if a population is NOT in HWE, then one of the assumptions must be violated.

Modern Evolutionary Biology I. Population GeneticsA. OverviewB. The Genetic Structure of a PopulationC. The Hardy-Weinberg Equilibrium ModelD. Deviations from HWE 1. mutation

1. Consider a population with:

f(A) = p = 0.6 f(a) = q = 0.4

2. Suppose 'a' mutates to 'A' at a realistic rate of:

μ = 1 x 10-5

3. Well, what fraction of alleles will change?

'a' will decline by: qm = .4 x 0.00001 = 0.000004

'A' will increase by the same amount.

f(A) = p1 = 0.600004 f(a1) = q = 0.399996

p1 = 0.2

q1 = 0.8

p2 = 0.7

q2 = 0.3

Modern Evolutionary Biology I. Population GeneticsA. OverviewB. The Genetic Structure of a PopulationC. The Hardy-Weinberg Equilibrium ModelD. Deviations from HWE 1. mutation 2. migration

suppose migrants immigrate at a rate such that the new immigrants represent 10% of the new population

p2 = 0.7

q2 = 0.3p1 = 0.2

q1 = 0.8

Modern Evolutionary Biology I. Population GeneticsA. OverviewB. The Genetic Structure of a PopulationC. The Hardy-Weinberg Equilibrium ModelD. Deviations from HWE 1. mutation 2. migration

M = 10%

p(new) = p1(1-m) + p2(m)

= 0.2(0.9) + 0.7(0.1)

= 0.18 + 0.07 = 0.25

AA Aa aa

0.2 0.6 0.2

offspring

F1

D. Deviations from HWE 1. mutation 2. migration 3. Non-random Mating

a. Positive Assortative Mating – “Like mates with Like”

AA Aa aa

0.2 0.6 0.2

offspring ALL AA 1/4AA:1/2Aa:1/4aa ALL aa

F1



AA Aa aa

0.2 0.6 0.2

offspring ALL AA 1/4AA:1/2Aa:1/4aa ALL aa

0.2 0.15 + 0.3 + 0.15 0.2

F1 0.35 0.3 0.35




a. Positive Assortative Mating – “Like mates with Like”b. Inbreeding: Mating with Relatives

Decreases heterozygosity across the genome, at a rate dependent on the degree of relatedness among mates.

D. Deviations from HWE 1. mutation 2. migration 3. Non-random Mating 4. Finite Population Sizes: Genetic Drift

The organisms that actually reproduce in a population may not be representative of the genetics structure of the population; they may vary just due to sampling error

1 - small pops will differ more, just by chance, from the original population


1 - small pops will differ more, just by chance, from the original population

2 - small pops will vary more from one another than large


- “Founder Effect”

The Amish, a very small, close-knit group decended from an initial population of founders, has a high incidence of genetic abnormalities such as polydactyly


- “Founder Effect” and Huntington’s ChoreaHC is a neurodegenerative disorder caused by an autosomal lethal dominant allele.

The fishing villages around Lake Maracaibo in Venezuela have the highest incidence of Huntington’s Chorea in the world, approaching 50% in some communities.



The gene was mapped to chromosome 4, and the HC allele was caused by a repeated sequence of over 35 “CAG’s”. Dr. Nancy Wexler found homozygotes in Maracaibo and described it as the first truly dominant human disease (most are incompletely dominant and cause death in the homozygous condition).



By comparing pedigrees, she traced the incidence to a single woman who lived 200 years ago. When the population was small, she had 10 children who survived and reproduced. Folks with HC now trace their ancestry to this lineage.

- “Genetic Bottleneck”If a population crashes (perhaps as the result of a plague) there will be both selection and drift. There will be selection for those resistant to the disease (and correlated selection for genes close to the genes conferring resistance), but there will also be drift at other loci simply by reducing the size of the breeding population.

European Bison, hunted to 12 individuals, now number over 1000.

Cheetah have very low genetic diversity, suggesting a severe bottleneck in the past. They can even exchange skin grafts without rejection…

Elephant seals fell to 100’s in the 1800s, now in the 100,000’s

http://en.wikipedia.org/wiki/File:Male,_female_and_pup_Mirounga_angustirostris_20.jpg

Modern Evolutionary Biology

I. Population Genetics

A. Overview

B. The Genetic Structure of a Population

C. The Hardy-Weinberg Equilibrium Model

D. Deviations From HWE:

1. Mutation

2. Migration

3. Non-Random Mating:

4. Populations of Finite Size and Sampling Error - "Genetic Drift"

5. Natural Selection

1. Fitness Components:



1. Fitness Components:Fitness = The mean number of reproducing offspring / genotype

- probability of surviving to reproductive age - number of offspring - probability that offspring survive to reproductive age





2. Constraints:

i. finite energy budgets and necessary trade-offs:





2. Constraints:


GROWTH

METABOLISM

REPRODUCTION

Maximize probability of survival

GROWTH

METABOLISM

REPRODUCTION

GROWTH

METABOLISM

REPRODUCTION

Maximize reproduction



1. Fitness Components:2. Constraints:


TRADE OFF #1: Survival vs. Reproduction

METABOLISM

METABOLISMREPRODUCTION REPRODUCTION

Lots of small, low prob of survival

A few large, high prob of survival





TRADE OFF #1: Survival vs. ReproductionTRADE OFF #2: Lots of small offspring vs. few large offspring




i. finite energy budgets and necessary trade-offs:ii. Contradictory selective pressures:

Leaf Size

Photosynthetic potential

Water Retention





Leaf Size


Water Retention

Rainforest understory – dark, wet

Big leaves adaptive





Leaf Size


Water Retention

Desert – sunny, dry

Small leaves adaptive



1. Fitness Components:2. Constraints:3. Modeling Selection:

a. Calculating relative fitness

p = 0.4, q = 0.6 AA Aa aa

Parental "zygotes" 0.16 0.48 0.36 = 1.00

prob. of survival (fitness) 0.8 0.4 0.2

Relative Fitness 0.8/0.8=1 0.4/0.8 = 0.5 0.2/0.8=0.25

p = 0.4, q = 0.6 AA Aa aa

Parental "zygotes" 0.16 0.48 0.36 = 1.00

prob. of survival (fitness) 0.8 0.4 0.2

Relative Fitness 1 0.5 0.25

Survival to Reproduction 0.16 0.24 0.09 = 0.49

Freq’s in Breeding Adults 0.16/0.49 = 0.33

0.24/0.49 = 0.49

0.09/0.49 = 0.18

= 1.00

Gene Frequencies F(A) = 0.575 F(a) = 0.425

Freq’s in F1 (p2, 2pq, q2) 0.33 0.49 0.18 = 1.00



1. Fitness Components:2. Constraints:3. Modeling Selection:

a. Calculating relative fitnessb. Modeling Selection

Sources of Variation Agents of Change

Mutation Natural Selection

Recombination Genetic Drift

- crossing over Migration

- independent assortment Mutation

Non-random Mating

VA

RIA

TIO

N

Modern Evolutionary Biology

I. Population GeneticsA. OverviewB. The Genetic Structure of a PopulationC. The Hardy-Weinberg Equilibrium ModelD. Deviations From HWEE. Summary; The Modern Synthetic Theory of Evolution

Heredity, Gene Regulation, and Development

I. Mendel's ContributionsII. Meiosis and the Chromosomal TheoryIII. Allelic, Genic, and Environmental InteractionsIV. Sex Determination and Sex LinkageV. LinkageVI. MutationVII. Gene Regulation

Heredity, Gene Regulation, and Development

I. Mendel's ContributionsII. Meiosis and the Chromosomal TheoryIII. Allelic, Genic, and Environmental InteractionsIV. Sex Determination and Sex LinkageV. LinkageVI. MutationVII. Gene RegulationA. Overview

All cells in an organism contain the same genetic information; the key to tissue specialization is gene regulation – reading some genes in some cells and other genes in other cells.

VII. Gene RegulationA. Overview

All cells in an organism contain the same genetic information; the key to tissue specialization is gene regulation – reading some genes in some cells and other genes in other cells.

B. Terminology

Inducers turn a gene on…Repressors turn a gene off…

An “operon” is a region of genes that are regulated as a unit – it typically encodes > 1 protein involved in a particular metabolic pathway.

VII. Gene RegulationC. The lac Operon in E. coli


When lactose is present, E. coli produce three enzymes involved in lactose metabolism. Lactose is broken into glucose and galactose, and galactose is modified into glucose, too. Glucose is then metabolized in aerobic respiration pathways to harvest energy (ATP). When lactose is absent, E. coli does not make these enzymes and saves energy and amino acids.

How do these little bacteria KNOW? : )

Lac Y - permease – increases absorption of lactose

Lac Z – B-galactosidase – cleaves lactose into glucose and galactose

Lac A – transacetylase – may code for enzymes that detoxify waste products of lactose metabolism.



1960 – Jacob and Monod proposed that this was an inducible system under negative control. (Because the presence of the substrate INDUCES transcription by SHUTTING OFF regulation).

Repressor RNA Poly

Repressor Gene

Operator



LACTOSE



LACTOSE

The binding of lactose changes the shape of the repressor (allosteric reaction) and it can’t bind to the operator.


So, there are lots of genes that produce “regulatory proteins” which bind to other genes, and influence whether those genes are turned on and off.

This allows cells to become very different from one another, with certain subsets of genes turned on in some cells and off in others.

sources of variationagents of change mutationn.s. recombinationdrift - crossing overmigration -...

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population geneticsa

finite population sizes

genetic structure

positive assortative

nonrandom matinga

migration p2

initial population of

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