Drosophila immunity: QTL mapping, genetic variation and molecular evolution
Abstract
Drosophila is involved in a wide range of interactions with parasites
and pathogens (parasitoid wasps, bacteria, fungi, viruses). Drosophila
hosts vary greatly at the species, population and individual level, in
their response against such organisms, and much of this variation
has a genetic basis. In this thesis I explored three aspects of this
variation.
First, using recombination mapping based on SNPs and a variation
of bulk segregant analysis, I identified a QTL region on the right arm
of the third chromosome of D. melanogaster associated with resistance
to at least some of the parasitoid species / strains used in the
experiments. The location of the QTL was further explored with
deficiency complementation mapping and was narrowed down to
the 96D1-97B1 region. The success of the deficiency mapping
suggests that the resistant allele is not completely dominant.
Second, I investigated patterns of molecular evolution in a set of
immunity-related genes, using sequences from a D. melanogaster and
a D. simulans population and a set of genes without known
involvement in immunity for comparison. I found evidence that
several of these genes have evolved under different selection
pressure in each species, possibly indicating interactions with
different parasites. The immunity genes tested appear to be evolving
faster compared to non-immunity genes, supporting the idea that the
immune system is evolving under strong selective pressure from
parasites. Finally, in a D. melanogaster – sigma virus system, I measured genetic
variation in the transmission of different virus genotypes, in different
environments. There was poor correlation between temperatures,
suggesting that environmental heterogeneity could constraint
evolution of resistance (to virus transmission). The correlation
between viral genotypes was also low, although relatively stronger
for more closely phylogenetically related viral strains. Such
interactions between host genotypes, virus genotypes and
environmental conditions can maintain genetic variation in virus
transmission.