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RESEARCH INTERESTS
Evolutionary Biology
Experimental evolution of yeast in laboratory culture
Changes in fitness under relaxed selection
PUBLICATIONS
Evolution and Development
Changes in form occur both in the development of
individuals and in the evolution of species. Moreover, there
must be deep connections between change at those two
levels; morphological differences between adults of related
species must reflect accumulated modifications of
ancestral developmental programs. However, we know little
about the developmental basis of morphological evolution.
What kinds of genes are altered and how do they modify
development? The extensively analyzed segmentation
pathway in Drosophila embryos provides a useful
model system. Known genes produce molecular prepatterns
that determine the locations of specialized structures on the
larval cuticle. Surprisingly, these prepatterns are extremely
similar in species that make rather different cuticles,
suggesting that evolution has occurred primarily in genes
and molecules that "interpret" the prepatterns. Hairs and
denticles, whose arrangement constitutes the clearest
manifestation of cuticle patterning, form around spikes of
cytoplasm supported by a scaffolding of cytoskeleton,
notably bundles of actin filaments. Both the placement and
the shapes of cuticular specializations are anticipated by
ordered actin bundles. A variety of associated proteins
organize and crosslink actin into bundles of various shapes
and sizes. These "helpers" may be among the components
that have changed during evolution.
Evolution of yeast in test tubes and on
petri plates
The rapid growth and large population sizes of yeast in
culture permit sensitive detection of small fitness
differences and, hence, direct experimental observations
relevant to a number of important issues in evolutionary
biology. Here are a couple of examples: 1) Cryptic genes.
Even in genetically well characterized organisms like yeast,
many genes discovered in complete genome sequences had
never been found by ordinary genetics, and targeted
mutation of these "new" genes often produces no evident
phenotype. "Cryptic" or "redundant" genes probably are at
least as common in higher eukaryotes, including humans.
What are they good for and how can they evolve? Some may
yield phenotypes under conditions not yet tested, but many
may just make small contributions to the efficiency or
reliability of routine functions under normal conditions.
"Marginal" improvements in fitness far too small to detect by
standard laboratory procedures are readily "seen" by natural
selection. We tested this idea in headtohead competition
experiments and found that mutant strains that appear to be
perfectly normal nevertheless "lose" to wild type in the
long term. 2) Loss of fitness in the absence of selection.
Natural selection can drive adaptive change, but its most
common effect is to eliminate harmful mutations. Knowing
the rate at which damage accumulates without "purifying
selection" is important for a number of aspects of
evolutionary theory (e.g., what good is sex?), but there are
few reliable measurements. The effects of selection are
eliminated in very small populations; instead, random chance
(drift) determines which genes persist and which are lost. We
can mimic this by repeatedly isolating clones grown from
single cells. After many such population bottlenecks, we can
return strains to a competitive environment and measure any
decline in fitness relative to a standard strain. The nature of
interactions among deleterious mutations (e.g., synergistic
loss of fitness) also can be investigated.
Selected Publications
Dickinson, W.J., Y. Yang, K. Schuske and M. Akam. 1993.
Conservation of molecular prepatterns during the evolution
of cuticle morphology in Drosophila larvae.
Evolution 47:1396-1406.
Dickinson, W.J. 1995. Molecules and morphology: where's
the homology? Trends Genet. 11:119-21.
Dickinson, W.J. and J.W. Thatcher. 1997. Morphogenesis of
denticles and hairs in Drosophila embryos:
involvement of actin-associated proteins that also affect
adult structures. Cell Motil Cytoskeleton 38:
9-21.
Thatcher, J.W., J.M. Shaw and W.J. Dickinson. 1998.
Marginal fitness contributions of nonessential genes in
yeast. Proc. Natl. Acad. Sci. U.S.A 95:253-7.
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