Conservation and Evolution of Cis-Regulatory Systems in Ascomycete Fungi

Relatively little is known about the mechanisms through which gene expression regulation evolves. To investigate this, we systematically explored the conservation of regulatory networks in fungi by examining the cis-regulatory elements that govern the expression of coregulated genes. We first identified groups of coregulated Saccharomyces cerevisiae genes enriched for genes with known upstream or downstream cis-regulatory sequences. Reasoning that many of these gene groups are coregulated in related species as well, we performed similar analyses on orthologs of coregulated S. cerevisiae genes in 13 other ascomycete species. We find that many species-specific gene groups are enriched for the same flanking regulatory sequences as those found in the orthologous gene groups from S. cerevisiae, indicating that those regulatory systems have been conserved in multiple ascomycete species. In addition to these clear cases of regulatory conservation, we find examples of cis-element evolution that suggest multiple modes of regulatory diversification, including alterations in transcription factor-binding specificity, incorporation of new gene targets into an existing regulatory system, and cooption of regulatory systems to control a different set of genes. We investigated one example in greater detail by measuring the in vitro activity of the S. cerevisiae transcription factor Rpn4p and its orthologs from Candida albicans and Neurospora crassa. Our results suggest that the DNA binding specificity of these proteins has coevolved with the sequences found upstream of the Rpn4p target genes and suggest that Rpn4p has a different function in N. crassa

Experimental test of the consequences of host-parasite coevolution of the nematode Caenorhabditis elegans and its microparasite Bacillus thuringiensis

Host-parasite coevolution, or the evolution of host defence and parasite counter defence is predicted to associate with high selection dynamics that are crucial for the evolution of a number of biological processes, such as fitness traits related to bothantagonists and the mechanisms generating fast genetic changes. The main objective of my PhD thesis is to enhance our understanding of host-parasite coevolution as a major selective force. Hence I addressed the complex set of the predicted evolutionary consequences that are unique to host-parasite coevolution, at both the phenotypic and molecular level, for both antagonists, and across time. I used an experimental evolution approach - under controlled laboratory conditions - using the nematode Caenorhabditis elegans as a model host, and the bacterium Bacillus thuringiensis as a model parasite. I optimized the selection protocol and multiple phenotypic measurements to compare the differences in the evolutionary outcomes between coevolution, one-sided evolution, and control conditions. After 28 host generations, I found that coevolution (i) causes reciprocal changes in both host resistance and pathogen virulence, (ii) affects their life history trade-offs, and (iii) produces patterns that are clearly different from one-sided adaptation and control conditions (Chapter I). In general the consequences of host-parasite coevolution were more pronounced in the parasite except for the patterns of temporal adaptations (Chapter I). Moreover, my results gave insights into the role of males and outcrossing in the evolution of the studied host-parasite interactions. I found an opposing interference of two selective forces that act either on the inter-species level (i.e., the high selective pressure that the antagonists exert on each other; Red Queen theory) or on the intra-species level (i.e., the differences in immunity among host genders; Bateman’s principle of immunity). Males showed higher pathogen susceptibility than hermaphrodites, thus limiting but not abolishing the potential for outcrossing and recombination for fast host adaptation (Chapter II). Finally, for the parasite, we identified genetic changes in: (i) genotype frequency, (ii) the presence or combination of cry toxins, and (iii) the presence and frequency of single nucleotide polymorphisms (SNPs). The molecular analysis was done across three time points over all replicate populations. We found that the overall parasite evolution is dominated by clonal selection followed or combined with the spread of individual mutations (Chapter III)

Evolution of female multiple mating : A quantitative model of the “sexually selected sperm” hypothesis

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