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Kämper J Kahmann R Bölker M Ma LJ Brefort T Saville BJ Banuett F Kronstad JW Gold SE Müller O Perlin MH Wösten HA de Vries R Ruiz-Herrera J Reynaga-Peña CG Snetselaar K McCann M Pérez-Martín J Feldbrügge M Basse CW Steinberg G Ibeas JI Holloman W Guzman P Farman M Stajich JE Sentandreu R González-Prieto JM Kennell JC Molina L Schirawski J Mendoza-Mendoza A Greilinger D Münch K Rössel N Scherer M Vranes M Ladendorf O Vincon V Fuchs U Sandrock B Meng S Ho EC Cahill MJ Boyce KJ Klose J 《Nature》2006,444(7115):97-101
Ustilago maydis is a ubiquitous pathogen of maize and a well-established model organism for the study of plant-microbe interactions. This basidiomycete fungus does not use aggressive virulence strategies to kill its host. U. maydis belongs to the group of biotrophic parasites (the smuts) that depend on living tissue for proliferation and development. Here we report the genome sequence for a member of this economically important group of biotrophic fungi. The 20.5-million-base U. maydis genome assembly contains 6,902 predicted protein-encoding genes and lacks pathogenicity signatures found in the genomes of aggressive pathogenic fungi, for example a battery of cell-wall-degrading enzymes. However, we detected unexpected genomic features responsible for the pathogenicity of this organism. Specifically, we found 12 clusters of genes encoding small secreted proteins with unknown function. A significant fraction of these genes exists in small gene families. Expression analysis showed that most of the genes contained in these clusters are regulated together and induced in infected tissue. Deletion of individual clusters altered the virulence of U. maydis in five cases, ranging from a complete lack of symptoms to hypervirulence. Despite years of research into the mechanism of pathogenicity in U. maydis, no 'true' virulence factors had been previously identified. Thus, the discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi. Genomic analysis is, similarly, likely to open up new avenues for the discovery of virulence determinants in other pathogens. 相似文献
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Sarparanta J Jonson PH Golzio C Sandell S Luque H Screen M McDonald K Stajich JM Mahjneh I Vihola A Raheem O Penttilä S Lehtinen S Huovinen S Palmio J Tasca G Ricci E Hackman P Hauser M Katsanis N Udd B 《Nature genetics》2012,44(4):450-5, S1-2
Limb-girdle muscular dystrophy type 1D (LGMD1D) was linked to chromosome 7q36 over a decade ago, but its genetic cause has remained elusive. Here we studied nine LGMD-affected families from Finland, the United States and Italy and identified four dominant missense mutations leading to p.Phe93Leu or p.Phe89Ile changes in the ubiquitously expressed co-chaperone DNAJB6. Functional testing in vivo showed that the mutations have a dominant toxic effect mediated specifically by the cytoplasmic isoform of DNAJB6. In vitro studies demonstrated that the mutations increase the half-life of DNAJB6, extending this effect to the wild-type protein, and reduce its protective anti-aggregation effect. Further, we show that DNAJB6 interacts with members of the CASA complex, including the myofibrillar myopathy-causing protein BAG3. Our data identify the genetic cause of LGMD1D, suggest that its pathogenesis is mediated by defective chaperone function and highlight how mutations in a ubiquitously expressed gene can exert effects in a tissue-, isoform- and cellular compartment-specific manner. 相似文献
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Rachel V Baxter Kamel Ben Othmane Julie M Rochelle Jason E Stajich Christine Hulette Susan Dew-Knight Faycal Hentati Mongi Ben Hamida S Bel Judy E Stenger John R Gilbert Margaret A Pericak-Vance Jeffery M Vance 《Nature genetics》2002,30(1):21-22
We previously localized and fine-mapped Charcot Marie Tooth 4A (CMT4A), the autosomal recessive, demyelinating peripheral neuropathy, to chromosome 8. Through additional positional cloning, we have identified a good candidate gene, encoding ganglioside-induced differentiation-associated protein-1 (GDAP1). We found three different mutations in four different Tunisian families-two nonsense and one missense mutation. How mutations in GDAP1 lead to CMT4A remains to be understood. 相似文献
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James TY Kauff F Schoch CL Matheny PB Hofstetter V Cox CJ Celio G Gueidan C Fraker E Miadlikowska J Lumbsch HT Rauhut A Reeb V Arnold AE Amtoft A Stajich JE Hosaka K Sung GH Johnson D O'Rourke B Crockett M Binder M Curtis JM Slot JC Wang Z Wilson AW Schüssler A Longcore JE O'Donnell K Mozley-Standridge S Porter D Letcher PM Powell MJ Taylor JW White MM Griffith GW Davies DR Humber RA Morton JB Sugiyama J Rossman AY Rogers JD Pfister DH Hewitt D Hansen K Hambleton S Shoemaker RA Kohlmeyer J 《Nature》2006,443(7113):818-822
The ancestors of fungi are believed to be simple aquatic forms with flagellated spores, similar to members of the extant phylum Chytridiomycota (chytrids). Current classifications assume that chytrids form an early-diverging clade within the kingdom Fungi and imply a single loss of the spore flagellum, leading to the diversification of terrestrial fungi. Here we develop phylogenetic hypotheses for Fungi using data from six gene regions and nearly 200 species. Our results indicate that there may have been at least four independent losses of the flagellum in the kingdom Fungi. These losses of swimming spores coincided with the evolution of new mechanisms of spore dispersal, such as aerial dispersal in mycelial groups and polar tube eversion in the microsporidia (unicellular forms that lack mitochondria). The enigmatic microsporidia seem to be derived from an endoparasitic chytrid ancestor similar to Rozella allomycis, on the earliest diverging branch of the fungal phylogenetic tree. 相似文献
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Fraser JA Giles SS Wenink EC Geunes-Boyer SG Wright JR Diezmann S Allen A Stajich JE Dietrich FS Perfect JR Heitman J 《Nature》2005,437(7063):1360-1364
Genealogy can illuminate the evolutionary path of important human pathogens. In some microbes, strict clonal reproduction predominates, as with the worldwide dissemination of Mycobacterium leprae, the cause of leprosy. In other pathogens, sexual reproduction yields clones with novel attributes, for example, enabling the efficient, oral transmission of the parasite Toxoplasma gondii. However, the roles of clonal or sexual propagation in the origins of many other microbial pathogen outbreaks remain unknown, like the recent fungal meningoencephalitis outbreak on Vancouver Island, Canada, caused by Cryptococcus gattii. Here we show that the C. gattii outbreak isolates comprise two distinct genotypes. The majority of isolates are hypervirulent and have an identical genotype that is unique to the Pacific Northwest. A minority of the isolates are significantly less virulent and share an identical genotype with fertile isolates from an Australian recombining population. Genotypic analysis reveals evidence of sexual reproduction, in which the majority genotype is the predicted offspring. However, instead of the classic a-alpha sexual cycle, the majority outbreak clone appears to have descended from two alpha mating-type parents. Analysis of nuclear content revealed a diploid environmental isolate homozygous for the major genotype, an intermediate produced during same-sex mating. These studies demonstrate how cryptic same-sex reproduction can enable expansion of a human pathogen to a new geographical niche and contribute to the ongoing production of infectious spores. This has implications for the emergence of other microbial pathogens and inbreeding in host range expansion in the fungal and other kingdoms. 相似文献
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