Fungal Genetics and Biology 44 (2007) 284–292 www.elsevier.com/locate/yfgbi 1087-1845/$ - see front matter  2006 Elsevier Inc. All rights reserved. doi:10.1016/j.fgb.2006.10.005 Origin and colonization history of newly virulent strains of the phytopathogenic fungus Venturia inaequalis Fabien Guérin 1 , Pierre Gladieux 1 , Bruno Le Cam ¤ UMR077 PAVE, INRA, F-49071 Beaucouze, France Received 27 April 2006; accepted 20 October 2006 Available online 12 December 2006 Abstract Plant resistance based on a gene-for-gene relationship tends not to be durable because virulent strains can emerge through mutation and colonize formerly resistant cultivars over large areas. Our objective was to determine the origin and colonization history of newly vir- ulent strains of the fungus Venturia inaequalis. Four hundred and eighty-one strains from seven multi-cultivar orchards within a 300 km wide area were collected from a cultivar carrying the overcome Vf-gene (Vfcv populations) and from non-Vf cultivars (nVfcv popula- tions). Using 9 microsatellite loci, we showed that Vfcv populations were closely related though highly diVerentiated, indicating they have been recently founded following rare long distance dispersal events from a common origin. Assignment tests revealed that the Vfcv popu- lations had not emerged from any of the nVfcv populations. Vfcv populations had a low diversity and were strongly diVerentiated from nVfcv populations several years after the Wrst reported breakdown, suggesting reproductive isolation between the two populations.  2006 Elsevier Inc. All rights reserved. Keywords: Resistance durability; Apple scab; Population structure; Multilocus microsatellite genotyping; Dispersal; Founder events 1. Introduction Plant resistance to fungal pathogens often depends on a gene-for-gene interaction (Flor, 1971). In this interaction, an avirulence (avr) gene in the pathogen controls a signal whose recognition by the plant requires a functional resis- tance (R) gene. Once the pathogen is recognized, an array of defence responses is triggered (Dangl and Jones, 2001; de Wit, 2002). For many cultivated species, resistances based on R genes have been favoured in selection by plant breed- ers because they provide a complete control of the disease. However, despite its great potential eYciency, a gene-for- gene resistance may be broken down, as a single mutation in the pathogen is suYcient to break the functionality of the avirulence gene, thereby changing the pathogen from aviru- lence to virulence (Schulze-Lefert et al., 1997). This vulnera- bility is increased by the spatial anthropogenic distribution of R genes in the landscape. New resistant cultivars are often grown homogeneously on large areas allowing newly virulent strains to initiate epidemics that will rapidly overcome a resistance that had been acquired after a long lasting breeding program (Brown, 1994). Two processes need to be investigated in order to improve the durability of a resistance: the changes leading to the loss of function of the avr gene and the spread of the virulent genotype. Cloning of avirulence genes in Rhynchos- porium secalis (Schurch et al., 2004), Leptosphaeria macu- lans (Attard et al., 2002; Gout, 2005) and Magnaporthe grisea (Farman et al., 2002; Fudal, 2005) allowed the deter- mination of the number of virulence acquisition events on world scale. If the avr gene is not yet cloned, a population genetics approach using neutral molecular markers is a powerful alternative. For example, such an approach has demonstrated that the breakdown of the Mla13 resistance gene to barley powdery mildew had been caused by two clones of Blumeria graminis f. sp. hordei (Brown, 1994). The mode of dispersal of virulent populations can also be inferred from the analysis of population structure. One * Corresponding author. Fax: +332 41 22 57 05. E-mail address: lecam@angers.inra.fr (B. Le Cam). 1 These authors contributed equally to this work.