movement (i.e. gene and genotype flow) can point to weak links in quarantine systems. We combined microsatellite and DNA sequence data from neutral RFLP loci and housekeeping genes with phylogenetic and coalescent analysis to infer the demographic history and paths of genetic exchange among 384 isolates of the wheat pathogen Mycosphaerella graminicola originating from 14 populations on four continents. Though this talk will focus on M. graminicola, the coalescent approaches should be applicable to any plant or animal pathogen, and can be applied in the context of biosecurity to determine sources of newly introduced pathogen populations, whether through increasing international travel and commerce, or through bioterrorism.
Comparing the Evolution of Genetic Variation at RFLP Loci and Quantitative Traits in the Pathogenic Fungus Mycosphaerella graminicola
Zhan, J. and B. A. McDonald, Institute of Plant Sciences, Phytopathology Group, ETH Zentrum / LFW, Universitätstrasse 2, CH-8092 Zürich, Switzerland
Determining genetic variation among populations and factors contributing to the origin, maintenance and distribution of the genetic variation has been a central theme for evolutionary study. This type of study is also of great interest to plant pathologists and breeders because understanding the evolution of genetic variation is critical for efficiently managing plant diseases and natural resources. Empirical studies related to evolution of genetic variation were surrogated with information derived from molecular genetic markers. In this study, we used the combination of molecular genetic tools and quantitative genetic approaches to compare genetic variation and population differentiation at RFLP marker loci and three quantitative loci (fungicide resistance, temperature sensitivity and colony size) in five Mycosphaerella graminicola populations sampled from different geographic regions. One population each was sampled from Australia, Israel and Switzerland and two populations were sampled from Oregon, USA. The two Oregon populations were collected on the same day from a field grown with two wheat cultivars differing in their level of resistance to M. graminicola. Our results revealed wide variations in the level of additive genetic variance, narrow sense heritability and population differentiation (QST) among the fungal populations across the three quantitative traits. The QST for fungicide resistance and temperature sensitivity were significant higher than GST for RFLP loci while the QST for colony size was not significantly different from the GST for the molecular markers. These results suggest that diversifying selection for local adaptation played a significant role in the evolution of fungicide resistance and temperature sensitivity while the major genetic forces governing the evolution of population differentiation in colony size were random drift and mutation. Further analysis revealed that the pathogen population from Switzerland displayed the highest level of fungicide resistance and the pathogen population from the resistant host displayed a significantly higher level of fungicide resistance than that from the susceptible host. Our results also revealed a positive and significant correlation between genetic variation in molecular marker loci and quantitative traits, suggesting that estimates of genetic variation at quantitative traits could be derived directly from molecular genetic markers, rather than through the complicated process of estimating additive genetic variance.
Plenary talk 3
Sequence-specific RNA degradation in resistance to plant viruses
Giovanni P. Martelli
Department of Plant Protection and Applied Microbiology, University of Bari and Institute of Plant Virology of CNR, Bari section, Italy
Plants resist viral infections through innate or adaptive responses. Innate responses are mediated by different mechanisms (e.g. lack of host-coded helper functions interacting with virus-coded pathogenicity factors, presence of antagonistic compounds or unsuitable chemical conditions of the host cells). Adaptive responses are exemplified by post-transcriptional gene silencing (PTGS), a mechanism whereby the sequence-specific degradation of target transcripts takes place in the cytoplasm of the host cells. PTGS is triggered by the presence of functional (genomic) or aberrant (transgenic) ssRNA transcripts that are recognized by an RNA-dependent RNA polymerase (RdRp) which can be coded by the host. Complementary RNA molecules are synthesized, which anneal with the template, yielding dsRNAs that are processed by a host-encoded dsRNase to small dsRNAs 21-25 nucleotides in size, referred to as small interfering RNAs (siRNAs). A mechanism is then activated, whereby all RNA molecules homologous to the double-stranded sequences are degraded.