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BACKGROUND: Resistance to rodenticides has been reported globally and poses a considerable problem for efficacy in pest control. The most-documented resistance to rodenticides in commensal rodents is associated with mutations in the Vkorc1 gene, in particular in codon 139. Resistance to anticoagulant rodenticides has been reported in the Netherlands since 1989. A study from 2013 showed that 25% of 169 Norway rats (Rattus norvegicus) had a mutation at codon 139 of the Vkorc1 gene. To gain insight in the current status of rodenticide resistance amongst R. norvegicus and house mice Mus musculus in the Netherlands, we tested these rodents for mutations in codon 139 of the Vkorc1 gene. In addition, we collected data from pest controllers on their use of rodenticides and experience with rodenticide resistance. RESULTS: A total of 1801 rodent samples were collected throughout the country consisting of 1404 R. norvegicus and 397 M. musculus. In total, 15% of R. norvegicus [95% confidence interval (CI): 13–17%] and 38% of M. musculus (95% CI: 33–43%) carried a genetic mutation at codon 139 of the Vkorc1 gene. CONCLUSION: This study demonstrates genetic mutations at codon 139 of the Vkorc1 gene in M. musculus in the Netherlands. Resistance to anticoagulant rodenticides is present in R. norvegicus and M. musculus in multiple regions in the Netherlands. The results of this comprehensive study provide a baseline and facilitate trend analyses of Vkorc1 codon 139 mutations and evaluation of integrated pest management (IPM) strategies as these are enrolled in the Netherlands.

Following earlier incomplete and fragmented versions of a genome sequence for the grey mould Botrytis cinerea, a gapless, near-finished genome sequence for B. cinerea strain B05.10 is reported. The assembly comprised 18 chromosomes and was confirmed by an optical map and a genetic map based on approximately 75 000 single nucleotide polymorphism (SNP) markers. All chromosomes contained fully assembled centromeric regions, and 10 chromosomes had telomeres on both ends. The genetic map consisted of 4153 cM and a comparison of the genetic distances with the physical distances identified 40 recombination hotspots. The linkage map also identified two mutations, located in the previously described genes Bos1 and BcsdhB, that conferred resistance to the fungicides boscalid and iprodione. The genome was predicted to encode 11 701 proteins. RNAseq data from >20 different samples were used to validate and improve gene models. Manual curation of chromosome 1 revealed interesting features, such as the occurrence of a dicistronic transcript and fully overlapping genes in opposite orientations, as well as many spliced antisense transcripts. Manual curation also revealed that the untranslated regions (UTRs) of genes can be complex and long, with many UTRs exceeding lengths of 1 kb and possessing multiple introns. Community annotation is in progress.

Mycosphaerella fijiensis (anamorph: Paracercospora fijiensis) is a hemibiotrophic fungal pathogen of banana and the causal agent of the devastating Black Sigatoka or black leaf streak disease. Its control frequently requires weekly fungicide applications when bananas are grown under disease-conducive conditions, which mostly represent precarious tropical environments. We started a multidisciplinary research program on M. fijiensis that is aiming at pesticide reduction. The first goal was to collect genomic data and to develop tools for molecular analysis of this pathosystem. These included the identification of the electrophoretic karyotype, construction of a high quality genetic linkage map and the sequencing of the entire genome. Here we review the current status of these approaches.

Mycosphaerella is one of the largest genera of plant pathogenic fungi with more than 1,000 named species, many of which are important pathogens causing leaf spotting diseases in a wide variety of crops including cereals, citrus, banana, eucalypts, soft fruits, and horticultural crops. A few species of Mycosphaerella cause disease in humans and other vertebrates. An international project was initiated to sequence the genomes of M. graminicola and M. fijiensis, two of the most economically important pathogens of wheat and banana, respectively, along with 40,000 ESTs from M. fijiensis and the related maize pathogen Cercospora zeae-maydis, through the Community Sequencing Program sponsored by the U.S. DOE-Joint Genome Institute. The 9x M. graminicola sequencing is complete and was made public November 1, 2006 following automated and manual annotation. Due to the very good assembly statistics as well as a >2000-marker DArT linkage map that was aligned to the genome, JGI decided to finish the M. graminicola genome at the Stanford Human Genome Center. The majority of chromosomes have been sequenced completely including both telomeres. These data indicate that M. graminicola has both the largest chromosome number and the smallest chromosome sizes recorded among filamentous ascomycetes. The M. fijiensis EST sequencing has resulted in more than 30,000 ESTs and the genome sequencing is currently at approximately 2.5x, which enabled us to revise the genome size estimate of M. fijiensis to approximately 68 Mb, which is 70% larger than that for M. graminicola. The current status of both sequencing projects will be discussed. (Texte intégral)