Book of Abstracts (PDF) - International Mycological Association

IMC7 Friday August 16th Lectures
367 - Selfish genes, sex and adaptation in yeast
M.R. Goddard
Centre for Population Biology, Imperial College at
Silwood Park, Ascot, U.K. - E-mail: m.goddard@ic.ac.uk
Most biologists agree that evolution occurs because those
members of a population best adapted to the current
environment will flourish at the expense of those less well
adapted. But what makes certain members of a population
better adapted? What is the link between genotype and
phenotype? How does this adaptation arise? The short
answer is by chance, random genetic mutations or novel
gene combinations will confer a greater fitness. But what
sort of mutations (e.g. duplications/point mutations), how
many mutations, does one mutation always win out or are
there many equally good solutions to a problem? I will
describe an experiment with asexual yeast which looks at
some of the mechanisms of adaptation to a saline
environment. The vast majority of organisms are sexual to
some degree, so how does sex affect adaptation? I will
describe a second experiment which tests the function of
sex - does it, as originally suggested, allow adaptation to
occur more rapidly? Lastly, even though sex has presumed
advantages, I will discuss some of the more unfortunate
consequences of sex - namely how it allows selfish or
parasitic genes to prosper.
368 - Mutation and selection in the yeast Saccharomyces
cerevisiae
R. Korona
Institute of Environmental Biology, Jagiellonian
University, Gronostajowa 3, 30-387 Krakow, Poland. - Email:
korona@eko.uj.edu.pl
Fitness of organisms is to a large extent determined by
quantitative traits, such as growth rate. The study of
mutation affecting such traits is impeded by the fact that
individual alleles often cause small and recessive effects.
Fungal experimental systems, such as laboratory
populations of baker's yeast, provide unparalleled
opportunities for detection of new alleles. One reason is
that mutations can be studied both in haploids and diploids,
the other is the ease of propagation and growth rate assays.
We screened for mutations that appeared in diploids and
therefore were initially masked by wild-types but then,
after tetrad dissection analysis, were revealed as growth
defective haploids. We found that a deleterious or lethal
mutation occurs spontaneously at a rate of about one per
thousand of diploid genome replications. This seemingly
slow pace of mutation rate in unicellular organisms with
small genomes becomes substantial when extrapolated for
species that have several times larger genomes and many
cell replications per sexual generation. The collected
mutations were subsequently assayed for their dominance
and epistatic interactions (the latter only for non-lethals).
Heterozygous effects of lethals and non-lethals were very
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Book of Abstracts
small and equal on average which means that the former
were much better masked. Non-lethal mutations in
heterozygous loci interacted mostly multiplicatively
suggesting that neither their synergism nor antagonism
were strong.
369 - Evolution of azole resistance in yeasts: Genetics
and genomics
L.E. Cowen * , L.M. Kohn & J.B. Anderson
Department of Botany, University of Toronto, 3359
Mississauga Road North, Mississauga, Ontario, L5L 1C6,
Canada. - E-mail: lcowen@utm.utoronto.ca
We established twelve replicate experimental populations
of Candida albicans to study the dynamics and
mechanisms of adaptation to the azole antifungal agents.
The experimental populations were founded from a single
drug-sensitive cell; six populations were evolved with
inhibitory concentrations of fluconazole and six were
evolved without drug, over 330 generations. While all
populations evolved with fluconazole adapted to the
presence of drug, they followed strikingly different
trajectories. The experimental populations also diverged in
fitness. We measured changes in genome-wide gene
expression that became entrenched during adaptation and
persisted in the absence of drug using DNA microarrays.
Cluster analysis of the 301 genes with significantly
modulated expression identified three patterns of
adaptation to drug. One pattern was unique to one
population and included upregulation of the ABC
transporter gene, CDR2. A second pattern occurred at a late
stage of adaptation in three populations; for two of these
populations profiled earlier in their evolution, a different
pattern was observed at an early stage of adaptation. The
succession of early- and late-stage patterns of gene
expression, both of which include upregulation of the
major facilitator gene, MDR1, must represent a common
program of adaptation to this antifungal drug. We compare
these results with the dynamics and mechanisms of evolved
fluconazole resistance in experimental populations of
Saccharomyces cerevisiae.
370 - Predicting the evolutionary potential of plant
pathogenic fungi: a model framework
B.A. McDonald * & C.C. Linde
Institute of Plant Science, ETH Zurich, Universitatstrasse
2, Zurich CH-8049, Switzerland. - E-mail:
bruce.mcdonald@ipw.agrl.ethz.ch
Plant pathogenic fungi are notorious for evolving rapidly in
agroecosystems. Hence they offer good models for studies
in experimental population genetics and evolution.
Interactions among five population genetic forces
(mutation, migration, selection, drift, recombination)
ultimately affect the evolutionary potential of fungal