镰菌属的真菌是重要的植物病原体，引起各种各样的疫病、烂根或枯萎。有些菌种宿主选择范围很宽，而有些则选择范围较窄。对三个宿主选择范围有宽有窄的镰菌属真菌（其中两个刚完成测序）所做的比较基因组研究，为了解是什么驱动这些差异的提供了线索。
后续实验工作表明，仅仅将两个菌种在标准生长介质上混合（将来自一个尖孢镰刀菌番茄病原体的两个完整染色体转移），就能将一个非致病菌种变成一个致病菌种。这些发现为了解宿主范围及致病性的演化提供了线索。(生物谷Bioon.com)
生物谷推荐原文出处：
Nature doi:10.1038/nature08850
Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium
Li-Jun Ma1,26, H. Charlotte van der Does2,26, Katherine A. Borkovich3, Jeffrey J. Coleman4, Marie-Josée Daboussi5, Antonio Di Pietro6, Marie Dufresne5, Michael Freitag7, Manfred Grabherr1, Bernard Henrissat8, Petra M. Houterman2, Seogchan Kang9, Won-Bo Shim10, Charles Woloshuk11, Xiaohui Xie12, Jin-Rong Xu11, John Antoniw13, Scott E. Baker14, Burton H. Bluhm11, Andrew Breakspear15, Daren W. Brown16, Robert A. E. Butchko16, Sinead Chapman1, Richard Coulson17, Pedro M. Coutinho8, Etienne G. J. Danchin8,27, Andrew Diener18, Liane R. Gale15, Donald M. Gardiner19, Stephen Goff20, Kim E. Hammond-Kosack13, Karen Hilburn15, Aurélie Hua-Van5, Wilfried Jonkers2, Kemal Kazan19, Chinnappa D. Kodira1,27, Michael Koehrsen1, Lokesh Kumar1, Yong-Hwan Lee21, Liande Li3, John M. Manners19, Diego Miranda-Saavedra22, Mala Mukherjee10, Gyungsoon Park3, Jongsun Park21, Sook-Young Park9,27, Robert H. Proctor16, Aviv Regev1, M. Carmen Ruiz-Roldan6, Divya Sain3, Sharadha Sakthikumar1, Sean Sykes1, David C. Schwartz23, B. Gillian Turgeon24, Ilan Wapinski1, Olen Yoder25, Sarah Young1, Qiandong Zeng1, Shiguo Zhou23, James Galagan1, Christina A. Cuomo1, H. Corby Kistler15 & Martijn Rep2
The Broad Institute, Cambridge, Massachusetts 02141, USA
University of Amsterdam, Amsterdam 1098XH, The Netherlands
University of California Riverside, California 92521, USA
University of Arizona, Tucson, Arizona 85721, USA
Université Paris-Sud, 91405 Paris, France
Universidad de Cordoba, Cordoba 14071, Spain
Oregon State University, Corvallis, Oregon 97331, USA
CNRS, Universités Aix-Marseille, 13628 Aix-en-Provence, France
Penn State University, University Park, Pennsylvania 16802, USA
Texas A&M University, College Station, Texas 77843, USA
Purdue University, West Lafayette, Indiana 47907, USA
University of California, Irvine, California 92697, USA
Centre for Sustainable Pest and Disease Management, Rothamsted Research, Harpenden AL5 2JQ, UK
Pacific Northwest National Laboratory, Richland, Washington 99352, USA
USDA ARS, University of Minnesota, St. Paul, Minnesota 55108, USA
USDA-ARS-NCAUR, Peoria, Illinois 61604, USA
European Bioinformatics Institute, Cambridge CB10 1SD, UK
University of California, Los Angeles, California 90095, USA
CSIRO Plant Industry, Queensland Bioscience Precinct, St Lucia, Brisbane, Queensland, 4067 Australia
BIO5 Institute, University of Arizona, Tucson, Arizona 85721, USA
Seoul National University, Seoul 151-742, Korea
Cambridge Institute for Medical Research, Cambridge CB2 0XY, UK
University of Wisconsin-Madison, Madison, Wisconsin 53706 USA
Cornell University, Ithaca, New York 14853, USA
17885 Camino Del Roca, Ramona, California 92065, USA
These authors contributed equally to this work.
Present addresses: 454 Life Sciences, Branford, Connecticut 06405, USA (C.D.K.); University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390, USA (L.L.); INRA, Institut National de la Recherche Agronomique, 06903 Sophia-Antipolis, France (E.G.J.D.); Seoul National University, Seoul 151-742, Korea (S.-Y.P.).
Fusarium species are among the most important phytopathogenic and toxigenic fungi. To understand the molecular underpinnings of pathogenicity in the genus Fusarium, we compared the genomes of three phenotypically diverse species: Fusarium graminearum, Fusarium verticillioides and Fusarium oxysporum f. sp. lycopersici. Our analysis revealed lineage-specific (LS) genomic regions in F. oxysporum that include four entire chromosomes and account for more than one-quarter of the genome. LS regions are rich in transposons and genes with distinct evolutionary profiles but related to pathogenicity, indicative of horizontal acquisition. Experimentally, we demonstrate the transfer of two LS chromosomes between strains of F. oxysporum, converting a non-pathogenic strain into a pathogen. Transfer of LS chromosomes between otherwise genetically isolated strains explains the polyphyletic origin of host specificity and the emergence of new pathogenic lineages in F. oxysporum. These findings put the evolution of fungal pathogenicity into a new perspective.
