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Poster Full Abstracts - Evolution and Quantitative Genetics
Poster board number is above title. The first author is the presenter
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same roles in the different Drosophila species; in particular we are testing whether Distal-less has been repeatedly co-opted to orchestrate the expression of
the same effectors in a spot like pattern.
449B
Forces shaping a Hox morphogenetic gene-network during evolution.
James Castelli-Gair Hombria, Sol Sotillos, Mario Aguilar, Filippo Foglia. CABD,
CSIC/JA/UPO, Seville, Sevilla, Spain.
The Abdominal-B selector protein induces the organogenesis of the posterior spiracles by coordinating an organ specific gene-network. The complexity of
this network begs the question of how it originated during posterior spiracle evolution and what were the selective pressures driving its formation. As the
network probably formed piecemeal with elements being recruited sequentially during evolution, we studied the morphogenetic consecuences of expressing
in naive epithelial cells individual effector targets of the posterior spiracle network. In most cases, single target expression has little morphogenetic effect. In
contrast, expression of the Cv-c RhoGAP protein increases actin based motility but also leads to epithelial polarity and adhesion defects. We show that these
defects do not occur in spiracle cells normally expressing Cv-c because they have developed compensatory mechanisms. These mechanisms include the
organ specific upregulation of cell polarity and adhesion molecules, which help compensating the deleterious effects caused by the transient Cv-c induced
Rho1 inactivation. We show that other epithelial cells like the salivary gland, the leading edge and the trachea which also have coopted Cv-c to their
morphogenetic gene-networks are also resistant to Cv-c’s deleterious effects on adhesion and epithelial polarity. We suggest that during evolution, Cv-c
recruitment to any epithelium would have caused similar defects that resulted in a strong selective pressure that necessarily lead to recruit in those same cells
downstream targets involved in the control of basic cell properties (adhesion and polarity regulators) to regain homeostasis. We propose based on our data,
that when a selector gene cascade coopts a morphogenetic regulator, the instability caused requires the recruitment of various compensatory molecules that
normalize it.
450C
vestigial
ectodermal function is not limited to wing development in
Tribolium
.
Courtney M. Clark, Yoshinori Tomoyasu. Zoology Department, Miami
University, Oxford, OH.
The
vestigial
gene (
vg
) is often referred to as a wing “master gene” because of its ability to induce wings in various locations in
Drosophila
when it is
overexpressed. The ectodermal function of
vg
in
Drosophila
seems to be limited to wing formation. However, it is yet to be determined to what extent the
function of
vg
is conserved among other insect species. We disrupted the
vg
function via RNA interference (RNAi) in the red flour beetle,
Tribolium
casteneum
, and analyzed the phenotypes. Depletion of
vg
in the late larval stages led to a partial or entire deletion of the hindwings and elytra. Interestingly,
we also found that
vg
RNAi induced novel body wall phenotypes in the first and third thoracic segments. We analyzed the
vg
RNAi phenotypes in
Drosophila
, and confirmed that the function of
vg
in flies is limited to wing development. Expression analysis has revealed that
vg
is expressed not only in
dorsal appendage primordia, but also is expressed broadly throughout the thoracic and abdominal segments of the developing embryo of both
Drosophila
and
Tribolium
. Recently, it has been reported that
vg
is expressed in the body wall of bristletails, which do not possess wings (Niwa et al, 2010). These
results suggest that unlike in
Drosophila
,
vg
function in the ectoderm is not limited to wing development in
Tribolium
and that
vg
has an important role in
insect body wall development that has been lost in
Drosophila
.
Current evo-devo research using
Drosophila
studies as a paradigm has been quite successful for understanding the changes that have contributed to
morphological evolution. However, this approach has a caveat of creating a fly-biased view of evolution. Our study shows the importance of analyzing gene
function in organisms other than
Drosophila
to gain a more comprehensive view of morphological evolution.
451A
Modeling allometry using lessons from
Drosophila
.
Austin P. Dreyer, Eli M. Swanson, Alexander W. Shingleton. Dept Zoology, Michigan State Univ,
East Lansing, MI.
How natural selection alters scaling relationships among traits, called allometries, is a poorly understood question in evolution. Elucidating the evolution of
allometries, however, is fundamental to understanding how morphological variation is generated and maintained. Though many scaling relationships are
undoubtedly the result of selection, questions remain about which types of selection generate which allometric relationships. Specifically, it is unclear which
selection regimes would tend to increase or decrease the extent to which one trait scales with another among members of a population. Such questions are
exceedingly difficult to test with any degree of power in living systems. To circumvent this problem we used mathematical models to simulate the effect of
different forms of selection on scaling relationships. The model is based on the developmental and genetic mechanisms that regulate body and organ size in
Drosophila
. Using this method we are able to test for the theoretical conditions that give rise to isometry, where organs maintain proportionality as they
increase in size, hyperallometry, where one organ becomes proportionally larger in relation to another as they both increase in size, and hypoallometry,
where one organ becomes proportionally smaller in relation to another as they both increase in size. We demonstrate that selection on the two traits
concurrently results in more rapid responses in the slope of the scaling relationship than selection on any one of the traits alone. The results of the model
allow us to make predictions about the nature of selection on scaling relationships and the nature of the mechanisms targeted by selection.
452B
Expression and Function of
fushi tarazu
in Diptera.
Amanda Field, Leslie Pick. University of Maryland, 4112 Plant Sciences Building, College Park,
MD.
Highly conserved regulatory genes direct body patterning of diverse animals. How these regulatory networks have evolved to direct the development of
different body plans is a fundamental question in the evo-devo field. Two homeodomain genes, ftz and Antp, evolved from a common ancestral Hox gene.
While Antp remained well conserved throughout arthropods, ftz rapidly evolved from a Hox gene in more basal arthropods to a pair-rule segmentation gene
in Drosophila melanogaster. Changes in ftz function resulted from variations in its expression pattern and in its protein coding sequence, the latter leading to
the acquisition of a new protein partner for Dm-Ftz, the orphan nuclear receptor Ftz-F1. Critical changes in ftz appear to have occurred at the base of insect
radiation, in the holometabolous stem group and in Diptera (Heffer et al. 2010). Drosophila melanogaster and the dengue and yellow-fever vector mosquito,
Aedes Aegypti, represent distant dipteran lineages, providing an opportunity to assess whether and to what extent the functions of ftz and Antp have