MENDELIAN GENETICS IN

POPULATIONS I: SELECTION
AND MUTATION 4

April 26, 1986 @ 0123

In Ukarine

reactor 4 meltdown
nuclear meltdown

131Ilevels
review; include mutation in HWCE treatment
elevated 137Cs
for detected in Sweden
population geneticson April 27
Iodine levels are indictative of nuclear meltdown
QUICKTHINK
Cavener and Clegg (1981) exposed two
laboratory Drosophila populations to two
different treatments, one containing a regular
fruit fly chow diet and another containing a
diet spiked with EtOH, and monitored two
alleles at the alcohol dehydrogenase locus,
AdhS and AdhF. Please review their data,
which will be presented in a moment, and
deduce which selection scheme type applied
to the populations.
 Figure 6-14

selection
QUICKTHINK
Dawson (1970) studied two laboratory
Tribolium populations in similar environments
and monitored two alleles at the l locus, + and
l, which is recessive and lethal in the
homozygous state. Please review the data,
which will be presented in a moment, and
deduce which selection scheme type applied
to the populations.
Figure 6-19

homozygomous have a
fitness have the lowest
fitness (0)
QUICKTHINK
Mukai and Burdick (1959) twice studied two
laboratory Drosophila populations in similar
environments and monitored two alleles at the
V/L locus, V and L, which is lethal in the
homozygous state. Please review the red
data, which will be presented in a moment,
and deduce which selection scheme type
applied to the populations.
 Figure 6-21

hetro is not disappearing as fast

other mechanism that retains the delertroius allele: underdominance

QUICKTHINK
Foster et al. (1959) studied 11 and 13
laboratory Drosophila populations with
compound chromosomes in similar
environments and effectively monitored two
alleles at a locus. Please review the data,
which will be presented in a moment, and
deduce which selection scheme type applied
to the populations.
 Figure 6-23

only 25% of the offspring pop would be viable

both graphs that disappear, have underdominance (one is symmetrical, the other isn't)
 example of negative frequency dependent selection because
the rarest one, gains fitness: e.g red in the feild of yellow
flowers Figure 6-24

f-DEPENDENT SELECTION
Another example is plant
self-incompatibility alleles.
When two plants share the
same incompatibility allele,
they are unable to mate.
Thus, a plant with a new (and
therefore, rare) allele has
more success at mating, and
its allele spreads quickly
through the population
 SECOND VIOLATION OF HW: OCCURANCE OF MUTATION
Figure 6-26

no reverse mutation: consider them negilible

MUTATION:mistake at the genetic level

MUTATION
converts one allele to another
(e.g., A to a)

p = p - p q = q + p

p = p - p = -
p is mutation rate(1/1000)
high mutation rate

dp / dg -
p e.g., = 10-4, p0 = 0.90

dp / p = -
dg n = 103, pn = 0.81

pn = p0 e- n
 Figure 6-27
mutation gradual
mutation does not produce drastic change over small
timeframe
 selection

mutation & s

jumps due to mutations However, mutation and selection can

occationally a down step produce drastic change over small
timeframe; especially prevalant in
populations with smaller generation
time

Inbreeding tends to decrease the

 Figure 6-28
EFFECT OF HIGH
SALT DIET
; very stressful essentially genetically identical
inbreeding tends to
decrease
genetic diversity -generated variation
this is why we have
laws aganist this
becuase could be
deleterious

-s-derived adaptation

salt - stressed lines could

handle stress better no migration
tried to minimize
natural selection
only mechanism
for variation: salt
diet and
mutations
MUTATION-SELECTION
DELETERIOUS RECESSIVE
w11 w12 w22
1 1 1-s

p* = p / (1 - s(1 - p)2)

p = (1 - ) p* = (1 - ) p / (1 - s(1 - p)2)
s =0; no fitness

p = p if (1 - p)2 = / s
equilibrium p*: frequency based on expected selection
scheme
MUTATION-SELECTION
LETHAL DOMINANT a2 allele is dominant

w11 w12 w22

1 0 0

p* = 1

p = (1 - )

p = p if (1 - p) =
 Figures 6-29, 6-30, 6-31

this regulator
allows the lungs
to digest the
bacteria that
causes the
infection; if you
lack this
receptor, like int
Cystic Fibrosis Transmembrane conductance Regulator he case of CF,
then you have
infection
Figures 6-29, 6-30, 6-31

why is then ppl who do not

have the allele are not
wiped out? Because of
heterozygote advantage.
Previously, ppl who lacked
the thing could survive
typhoid fever better;
therefore, this is a result of
previous selection.
 Figure 6-32
population genetics engineering test
artificial gene Medea
 Figure 6-33

population genetics engineering test

artificial gene Medea Punnett square
Figure 6-34
 Figure 6-35
population genetics engineering test
predictions & observations