Galagan J

References (5)

Title : Comparative genomics yields insights into niche adaptation of plant vascular wilt pathogens - Klosterman_2011_PLoS.Pathog_7_e1002137
Author(s) : Klosterman SJ , Subbarao KV , Kang S , Veronese P , Gold SE , Thomma BP , Chen Z , Henrissat B , Lee YH , Park J , Garcia-Pedrajas MD , Barbara DJ , Anchieta A , de Jonge R , Santhanam P , Maruthachalam K , Atallah Z , Amyotte SG , Paz Z , Inderbitzin P , Hayes RJ , Heiman DI , Young S , Zeng Q , Engels R , Galagan J , Cuomo CA , Dobinson KF , Ma LJ
Ref : PLoS Pathog , 7 :e1002137 , 2011
Abstract : The vascular wilt fungi Verticillium dahliae and V. albo-atrum infect over 200 plant species, causing billions of dollars in annual crop losses. The characteristic wilt symptoms are a result of colonization and proliferation of the pathogens in the xylem vessels, which undergo fluctuations in osmolarity. To gain insights into the mechanisms that confer the organisms' pathogenicity and enable them to proliferate in the unique ecological niche of the plant vascular system, we sequenced the genomes of V. dahliae and V. albo-atrum and compared them to each other, and to the genome of Fusarium oxysporum, another fungal wilt pathogen. Our analyses identified a set of proteins that are shared among all three wilt pathogens, and present in few other fungal species. One of these is a homolog of a bacterial glucosyltransferase that synthesizes virulence-related osmoregulated periplasmic glucans in bacteria. Pathogenicity tests of the corresponding V. dahliae glucosyltransferase gene deletion mutants indicate that the gene is required for full virulence in the Australian tobacco species Nicotiana benthamiana. Compared to other fungi, the two sequenced Verticillium genomes encode more pectin-degrading enzymes and other carbohydrate-active enzymes, suggesting an extraordinary capacity to degrade plant pectin barricades. The high level of synteny between the two Verticillium assemblies highlighted four flexible genomic islands in V. dahliae that are enriched for transposable elements, and contain duplicated genes and genes that are important in signaling/transcriptional regulation and iron/lipid metabolism. Coupled with an enhanced capacity to degrade plant materials, these genomic islands may contribute to the expanded genetic diversity and virulence of V. dahliae, the primary causal agent of Verticillium wilts. Significantly, our study reveals insights into the genetic mechanisms of niche adaptation of fungal wilt pathogens, advances our understanding of the evolution and development of their pathogenesis, and sheds light on potential avenues for the development of novel disease management strategies to combat destructive wilt diseases.
ESTHER : Klosterman_2011_PLoS.Pathog_7_e1002137
PubMedSearch : Klosterman_2011_PLoS.Pathog_7_e1002137
PubMedID: 21829347
Gene_locus related to this paper: vera1-c9srn2 , vera1-c9sn46 , verdv-g2wq49 , verdv-g2xca2 , vera1-c9sea3 , verdv-g2wzn4 , vera1-c9sek2 , verdv-g2wym5 , verdv-g2x5f3 , vera1-c9sx20 , vera1-c9sw01 , verdv-g2x1l1 , verdv-g2wuv4 , verdv-g2xaw5 , verdv-g2wsb2 , verdv-g2wty6 , vera1-c9si59 , verdv-g2xdu9 , vera1-c9s818 , verdv-g2xdr1 , verdv-g2wsw7 , verdv-g2wvq8 , 9pezi-a0a0g4li73 , vera1-kex1 , verdv-g2x8m5

Title : Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium - Ma_2010_Nature_464_367
Author(s) : Ma LJ , van der Does HC , Borkovich KA , Coleman JJ , Daboussi MJ , Di Pietro A , Dufresne M , Freitag M , Grabherr M , Henrissat B , Houterman PM , Kang S , Shim WB , Woloshuk C , Xie X , Xu JR , Antoniw J , Baker SE , Bluhm BH , Breakspear A , Brown DW , Butchko RA , Chapman S , Coulson R , Coutinho PM , Danchin EG , Diener A , Gale LR , Gardiner DM , Goff S , Hammond-Kosack KE , Hilburn K , Hua-Van A , Jonkers W , Kazan K , Kodira CD , Koehrsen M , Kumar L , Lee YH , Li L , Manners JM , Miranda-Saavedra D , Mukherjee M , Park G , Park J , Park SY , Proctor RH , Regev A , Ruiz-Roldan MC , Sain D , Sakthikumar S , Sykes S , Schwartz DC , Turgeon BG , Wapinski I , Yoder O , Young S , Zeng Q , Zhou S , Galagan J , Cuomo CA , Kistler HC , Rep M
Ref : Nature , 464 :367 , 2010
Abstract : 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.
ESTHER : Ma_2010_Nature_464_367
PubMedSearch : Ma_2010_Nature_464_367
PubMedID: 20237561
Gene_locus related to this paper: fusox-a0a1d3s5h0 , gibf5-fus2 , fusof-f9f2k2 , fusof-f9f3l6 , fusof-f9f6t8 , fusof-f9f6v2 , fusof-f9f132 , fusof-f9f781 , fusof-f9fd72 , fusof-f9fd90 , fusof-f9fem0 , fusof-f9fhk2 , fusof-f9fj19 , fusof-f9fj20 , fusof-f9fki8 , fusof-f9fmx2 , fusof-f9fnt4 , fusof-f9fpy4 , fusof-f9fvs6 , fusof-f9fwu0 , fusof-f9fxz4 , fusof-f9fzy5 , fusof-f9g2a2 , fusof-f9g3b1 , fusof-f9g5h7 , fusof-f9g6e6 , fusof-f9g6y7 , fusof-f9g7b0 , fusof-f9g797 , fusof-f9g972 , fusof-f9ga50 , fusof-f9gck4 , fusof-f9gd15 , gibze-a8w610 , gibze-b1pdn0 , gibze-i1r9e6 , gibze-i1rda9 , gibze-i1rdk7 , gibze-i1rec8 , gibze-i1rgs0 , gibze-i1rgy0 , gibze-i1rh52 , gibze-i1rhi8 , gibze-i1rig9 , gibze-i1rip5 , gibze-i1rpg6 , gibze-i1rsg2 , gibze-i1rv36 , gibze-i1rxm5 , gibze-i1rxp8 , gibze-i1rxv5 , gibze-i1s1u3 , gibze-i1s3j9 , gibze-i1s6l7 , gibze-i1s8i8 , gibze-i1s9x4 , gibze-q4huy1 , gibze-i1rg17 , fuso4-j9mvr9 , fuso4-j9ngs6 , fuso4-j9niq8 , fuso4-j9nqm2 , gibze-i1rb76 , gibze-i1s1m7 , gibze-i1s3z6 , gibze-i1rd78 , gibze-i1rgl9 , gibze-i1rjp7 , gibze-i1s1q6 , gibze-i1ri35 , gibze-i1rf76 , gibze-i1rhp3 , fusc1-n4uj11 , fusc4-n1s9p6 , gibf5-s0dqr2 , gibm7-w7n1b5 , fusof-f9g6q0 , gibm7-w7n497 , fusox-x0bme4 , gibm7-w7mcf8 , gibm7-w7mak5 , fusox-x0a2c5 , gibm7-w7mum7 , fusox-w9iyc7 , gibm7-w7maw6 , gibm7-w7msi0 , gibm7-w7luf0 , gibm7-w7msa3 , gibm7-w7mna8 , gibm7-w7n8b7 , gibm7-w7n564 , fusox-w9jpi0 , gibm7-w7ngc3 , gibm7-w7m4v6 , gibm7-w7m4v2 , gibm7-w7lt61 , gibm7-w7mly6 , gibm7-w7ncn3 , fusox-w9ibd7 , fusof-f9fnm6 , gibm7-w7n526 , gibza-a0a016pda4 , gibza-a0a016pl96 , gibm7-w7muq1 , fusof-f9gfd3 , gibm7-w7mt52 , gibze-i1rjb5 , gibf5-s0ehu3 , fusox-w9hvf0 , gibze-i1rkc4 , gibm7-w7mv30 , gibze-a0a1c3ylb1 , fuso4-a0a0c4diy4 , gibm7-w7n4n0 , gibze-gra11 , gibze-fsl2 , gibf5-fub4 , gibf5-fub5 , gibf5-fus5 , gibm7-dlh1

Title : Genomic analysis of the basal lineage fungus Rhizopus oryzae reveals a whole-genome duplication - Ma_2009_PLoS.Genet_5_e1000549
Author(s) : Ma LJ , Ibrahim AS , Skory C , Grabherr MG , Burger G , Butler M , Elias M , Idnurm A , Lang BF , Sone T , Abe A , Calvo SE , Corrochano LM , Engels R , Fu J , Hansberg W , Kim JM , Kodira CD , Koehrsen MJ , Liu B , Miranda-Saavedra D , O'Leary S , Ortiz-Castellanos L , Poulter R , Rodriguez-Romero J , Ruiz-Herrera J , Shen YQ , Zeng Q , Galagan J , Birren BW , Cuomo CA , Wickes BL
Ref : PLoS Genet , 5 :e1000549 , 2009
Abstract : Rhizopus oryzae is the primary cause of mucormycosis, an emerging, life-threatening infection characterized by rapid angioinvasive growth with an overall mortality rate that exceeds 50%. As a representative of the paraphyletic basal group of the fungal kingdom called "zygomycetes," R. oryzae is also used as a model to study fungal evolution. Here we report the genome sequence of R. oryzae strain 99-880, isolated from a fatal case of mucormycosis. The highly repetitive 45.3 Mb genome assembly contains abundant transposable elements (TEs), comprising approximately 20% of the genome. We predicted 13,895 protein-coding genes not overlapping TEs, many of which are paralogous gene pairs. The order and genomic arrangement of the duplicated gene pairs and their common phylogenetic origin provide evidence for an ancestral whole-genome duplication (WGD) event. The WGD resulted in the duplication of nearly all subunits of the protein complexes associated with respiratory electron transport chains, the V-ATPase, and the ubiquitin-proteasome systems. The WGD, together with recent gene duplications, resulted in the expansion of multiple gene families related to cell growth and signal transduction, as well as secreted aspartic protease and subtilase protein families, which are known fungal virulence factors. The duplication of the ergosterol biosynthetic pathway, especially the major azole target, lanosterol 14alpha-demethylase (ERG11), could contribute to the variable responses of R. oryzae to different azole drugs, including voriconazole and posaconazole. Expanded families of cell-wall synthesis enzymes, essential for fungal cell integrity but absent in mammalian hosts, reveal potential targets for novel and R. oryzae-specific diagnostic and therapeutic treatments.
ESTHER : Ma_2009_PLoS.Genet_5_e1000549
PubMedSearch : Ma_2009_PLoS.Genet_5_e1000549
PubMedID: 19578406

Title : Genome sequence of Aedes aegypti, a major arbovirus vector - Nene_2007_Science_316_1718
Author(s) : Nene V , Wortman JR , Lawson D , Haas B , Kodira C , Tu ZJ , Loftus B , Xi Z , Megy K , Grabherr M , Ren Q , Zdobnov EM , Lobo NF , Campbell KS , Brown SE , Bonaldo MF , Zhu J , Sinkins SP , Hogenkamp DG , Amedeo P , Arensburger P , Atkinson PW , Bidwell S , Biedler J , Birney E , Bruggner RV , Costas J , Coy MR , Crabtree J , Crawford M , Debruyn B , Decaprio D , Eiglmeier K , Eisenstadt E , El-Dorry H , Gelbart WM , Gomes SL , Hammond M , Hannick LI , Hogan JR , Holmes MH , Jaffe D , Johnston JS , Kennedy RC , Koo H , Kravitz S , Kriventseva EV , Kulp D , LaButti K , Lee E , Li S , Lovin DD , Mao C , Mauceli E , Menck CF , Miller JR , Montgomery P , Mori A , Nascimento AL , Naveira HF , Nusbaum C , O'Leary S , Orvis J , Pertea M , Quesneville H , Reidenbach KR , Rogers YH , Roth CW , Schneider JR , Schatz M , Shumway M , Stanke M , Stinson EO , Tubio JM , Vanzee JP , Verjovski-Almeida S , Werner D , White O , Wyder S , Zeng Q , Zhao Q , Zhao Y , Hill CA , Raikhel AS , Soares MB , Knudson DL , Lee NH , Galagan J , Salzberg SL , Paulsen IT , Dimopoulos G , Collins FH , Birren B , Fraser-Liggett CM , Severson DW
Ref : Science , 316 :1718 , 2007
Abstract : We present a draft sequence of the genome of Aedes aegypti, the primary vector for yellow fever and dengue fever, which at approximately 1376 million base pairs is about 5 times the size of the genome of the malaria vector Anopheles gambiae. Nearly 50% of the Ae. aegypti genome consists of transposable elements. These contribute to a factor of approximately 4 to 6 increase in average gene length and in sizes of intergenic regions relative to An. gambiae and Drosophila melanogaster. Nonetheless, chromosomal synteny is generally maintained among all three insects, although conservation of orthologous gene order is higher (by a factor of approximately 2) between the mosquito species than between either of them and the fruit fly. An increase in genes encoding odorant binding, cytochrome P450, and cuticle domains relative to An. gambiae suggests that members of these protein families underpin some of the biological differences between the two mosquito species.
ESTHER : Nene_2007_Science_316_1718
PubMedSearch : Nene_2007_Science_316_1718
PubMedID: 17510324
Gene_locus related to this paper: aedae-ACHE , aedae-ACHE1 , aedae-glita , aedae-q0iea6 , aedae-q0iev6 , aedae-q0ifn6 , aedae-q0ifn8 , aedae-q0ifn9 , aedae-q0ifp0 , aedae-q0ig41 , aedae-q1dgl0 , aedae-q1dh03 , aedae-q1dh19 , aedae-q1hqe6 , aedae-Q8ITU8 , aedae-Q8MMJ6 , aedae-Q8T9V6 , aedae-q16e91 , aedae-q16f04 , aedae-q16f25 , aedae-q16f26 , aedae-q16f28 , aedae-q16f29 , aedae-q16f30 , aedae-q16gq5 , aedae-q16iq5 , aedae-q16je0 , aedae-q16je1 , aedae-q16je2 , aedae-q16ks8 , aedae-q16lf2 , aedae-q16lv6 , aedae-q16m61 , aedae-q16mc1 , aedae-q16mc6 , aedae-q16mc7 , aedae-q16md1 , aedae-q16ms7 , aedae-q16nk5 , aedae-q16rl5 , aedae-q16rz9 , aedae-q16si8 , aedae-q16t49 , aedae-q16wf1 , aedae-q16x18 , aedae-q16xp8 , aedae-q16xu6 , aedae-q16xw5 , aedae-q16xw6 , aedae-q16y04 , aedae-q16y05 , aedae-q16y06 , aedae-q16y07 , aedae-q16y39 , aedae-q16y40 , aedae-q16yg4 , aedae-q16z03 , aedae-q17aa7 , aedae-q17av1 , aedae-q17av2 , aedae-q17av3 , aedae-q17av4 , aedae-q17b28 , aedae-q17b29 , aedae-q17b30 , aedae-q17b31 , aedae-q17b32 , aedae-q17bm3 , aedae-q17bm4 , aedae-q17bv7 , aedae-q17c44 , aedae-q17cz1 , aedae-q17d32 , aedae-q17g39 , aedae-q17g40 , aedae-q17g41 , aedae-q17g42 , aedae-q17g43 , aedae-q17g44 , aedae-q17gb8 , aedae-q17gr3 , aedae-q17if7 , aedae-q17if9 , aedae-q17ig1 , aedae-q17ig2 , aedae-q17is4 , aedae-q17l09 , aedae-q17m26 , aedae-q17mg9 , aedae-q17mv4 , aedae-q17mv5 , aedae-q17mv6 , aedae-q17mv7 , aedae-q17mw8 , aedae-q17mw9 , aedae-q17nw5 , aedae-q17nx5 , aedae-q17pa4 , aedae-q17q69 , aedae-q170k7 , aedae-q171y4 , aedae-q172e0 , aedae-q176i8 , aedae-q176j0 , aedae-q177k1 , aedae-q177k2 , aedae-q177l9 , aedae-j9hic3 , aedae-q179r9 , aedae-u483 , aedae-j9hj23 , aedae-q17d68 , aedae-q177c7 , aedae-q0ifp1 , aedae-a0a1s4fx83 , aedae-a0a1s4g2m0 , aedae-q1hr49

Title : Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis - Kamper_2006_Nature_444_97
Author(s) : Kamper J , Kahmann R , Bolker M , Ma LJ , Brefort T , Saville BJ , Banuett F , Kronstad JW , Gold SE , Muller O , Perlin MH , Wosten HA , de Vries R , Ruiz-Herrera J , Reynaga-Pena CG , Snetselaar K , McCann M , Perez-Martin J , Feldbrugge M , Basse CW , Steinberg G , Ibeas JI , Holloman W , Guzman P , Farman M , Stajich JE , Sentandreu R , Gonzalez-Prieto JM , Kennell JC , Molina L , Schirawski J , Mendoza-Mendoza A , Greilinger D , Munch K , Rossel N , Scherer M , Vranes M , Ladendorf O , Vincon V , Fuchs U , Sandrock B , Meng S , Ho EC , Cahill MJ , Boyce KJ , Klose J , Klosterman SJ , Deelstra HJ , Ortiz-Castellanos L , Li W , Sanchez-Alonso P , Schreier PH , Hauser-Hahn I , Vaupel M , Koopmann E , Friedrich G , Voss H , Schluter T , Margolis J , Platt D , Swimmer C , Gnirke A , Chen F , Vysotskaia V , Mannhaupt G , Guldener U , Munsterkotter M , Haase D , Oesterheld M , Mewes HW , Mauceli EW , Decaprio D , Wade CM , Butler J , Young S , Jaffe DB , Calvo S , Nusbaum C , Galagan J , Birren BW
Ref : Nature , 444 :97 , 2006
Abstract : 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.
ESTHER : Kamper_2006_Nature_444_97
PubMedSearch : Kamper_2006_Nature_444_97
PubMedID: 17080091
Gene_locus related to this paper: ustma-q4p4j7 , ustma-q4p5d2 , ustma-q4p8h8 , ustma-q4p8x7 , ustma-q4p082 , ustma-q4p194 , ustma-q4pa07 , ustma-q4pas0 , ustma-q4pbb4 , ustma-q4pg48