Zoology 445
Fall 2006
Conservation Genetics II: Handout
Reading: Johnson, JA, R Bellinger, JE Toepper and P Dunn (2004) Temporal change in allele
frequencies and low effective population size in greater prairie-chickens. Molecular Ecology 13:
2617 – 2630.
This paper tracks the change in genetic diversity of prairie-chickens populations in four protected
areas in Wisconsin. The paper investigates the change in diversity from the 1950s to the late
1990s. The authors also investigate the differentiation among these four protected areas using
FST. This is a challenging paper, but I suggest that you stick with it since it utilizes several
techniques, which we discussed in class, to determine the genetic vulnerability of prairie-chicken
populations in Wisconsin. The next section of this handout has some explanations and notes to
help you with the paper. Please refer to these notes and explanations while reading the paper.
Notes & explanations:
‘Focal’ population (page 2617) = sink population we discussed when we addressing species
distribution. We discussed that the checkerspot butterfly had a source-sink distribution.
The Materials and Methods section is daunting for someone not familiar with molecular
techniques. I suggest that you skip the subsections labeled ‘Tissue collection and DNA
extractions’ and ‘Genotyping and sequencing’. All you need to know for our purposes is that
the authors extracted DNA from prairie-chicken samples obtained in 1951 to 1954 and again in
1998 to 2000 for a time course analysis. The authors sequenced a 384 base pair region of the
mitochondrial DNA and determined the alleles at a series of “microsatellite” markers.
Microsatellite markers measure a highly variable part of the prairie-chicken genome.
I suggest that you glance over the subsection entitled ‘Statistical analyses’ (page 2619). The
authors describe how they calculate FIS (inbreeding coefficient = F I used in lecture) and FST.
Although their methods are more involved than our calculations, the FIS and FST values have the
same meaning as described in lecture and recitation. I also suggest that you glance at the
subsection entitled ‘Estimating Ne’ (page 2620). Again the techniques are more advanced
than anything we have done in class, but they are estimating Ne using the harmonic mean
method we discussed in lecture and by monitoring the decay in genetic variability to fit curves of
the theoretical decay of genetic variability at a particular effective population size (Ne). These
curves are similar in shape and trends to those shown at the top of page 4 of your genetic drift
handout; the figure in the handout is labeled Figure 11.5 (Futuyma). The curves used in the
paper differ from Figure 11.5 because mitochondria are haploid and maternally inherited.
Therefore they need to track decreases in variability of haplotypes. Each unique mitochondrial
DNA (mtDNA) sequence is called a haplotype, and drift is measured as the loss of haplotypes
from the population.
Results section: I ask that you concentrate on the results presented in Tables 1, 3, and 5. In
Table 1, larger values for mean alleles/locus, allelic richness, haplotype diversity and nucleotide
diversity always indicate more genetic variability. You should ignore material dealing with
Tajima’s D.
AM Jarosz
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Jarosz
Table 3 presents data for all possible pair wise comparison of populations using FST. From this
table you can compare a single population over time and space. For example you can compare
the Mead 1954 population with the 1998 population for the mitochondrial data by locating the
top row of data and looking at the FST value under Mead 1998 – 2000, which is 0.361. What
does this mean about the change in genetic structure over time? The value for the microsatellites
for the same comparison is found in the first column of data reading down to Mead 1998 – 2000,
which is 0.047. Why might these values differ so? Do you see the same pattern when
comparing the early samples with the later samples for the other three areas?
Table 5 provides estimates for effective population size (Ne) and migration rates (m) for the four
conservation areas. Why are the estimates of Ne larger when the authors assume no migration
(without migration in table)?
Questions:
1. On page 2618, the authors state: “Theoretically, because of its lek breeding behaviour
this species should be vulnerable to the effects of drift when population size is
significantly reduced.” Why does the lek breeding system increase the effects of genetic
drift?
2. What are the main trends in genetic variability based on the data in Table 1?
3. What are the main trends for population differentiation in Table 3?
a. Has the level of genetic differentiation changed among the four conservation
areas from the 1950s to the 1990s?
b. As mentioned above, the genetic differentiation over time in an area is more
pronounced in the mitochondrial data compared to the microsatellite data. What
pattern of migration might account for the difference between the mtDNA data
and the microsatellite data?
4. If the estimates of effective population size are indeed as low as 15 (see Table 5), what
implications does this have regarding the long-term viability of these populations?
5. The last paragraph of the paper discusses the need to maintain dispersal between local
populations. Why would migration help prevent extinction of these prairie-chicken
populations?
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