Sakthikumar S

References (4)

Title : Comparative genomic analysis of human fungal pathogens causing paracoccidioidomycosis - Desjardins_2011_PLoS.Genet_7_e1002345
Author(s) : Desjardins CA , Champion MD , Holder JW , Muszewska A , Goldberg J , Bailao AM , Brigido MM , Ferreira ME , Garcia AM , Grynberg M , Gujja S , Heiman DI , Henn MR , Kodira CD , Leon-Narvaez H , Longo LV , Ma LJ , Malavazi I , Matsuo AL , Morais FV , Pereira M , Rodriguez-Brito S , Sakthikumar S , Salem-Izacc SM , Sykes SM , Teixeira MM , Vallejo MC , Walter ME , Yandava C , Young S , Zeng Q , Zucker J , Felipe MS , Goldman GH , Haas BJ , McEwen JG , Nino-Vega G , Puccia R , San-Blas G , Soares CMF , Birren BW , Cuomo CA
Ref : PLoS Genet , 7 :e1002345 , 2011
Abstract : Paracoccidioides is a fungal pathogen and the cause of paracoccidioidomycosis, a health-threatening human systemic mycosis endemic to Latin America. Infection by Paracoccidioides, a dimorphic fungus in the order Onygenales, is coupled with a thermally regulated transition from a soil-dwelling filamentous form to a yeast-like pathogenic form. To better understand the genetic basis of growth and pathogenicity in Paracoccidioides, we sequenced the genomes of two strains of Paracoccidioides brasiliensis (Pb03 and Pb18) and one strain of Paracoccidioides lutzii (Pb01). These genomes range in size from 29.1 Mb to 32.9 Mb and encode 7,610 to 8,130 genes. To enable genetic studies, we mapped 94% of the P. brasiliensis Pb18 assembly onto five chromosomes. We characterized gene family content across Onygenales and related fungi, and within Paracoccidioides we found expansions of the fungal-specific kinase family FunK1. Additionally, the Onygenales have lost many genes involved in carbohydrate metabolism and fewer genes involved in protein metabolism, resulting in a higher ratio of proteases to carbohydrate active enzymes in the Onygenales than their relatives. To determine if gene content correlated with growth on different substrates, we screened the non-pathogenic onygenale Uncinocarpus reesii, which has orthologs for 91% of Paracoccidioides metabolic genes, for growth on 190 carbon sources. U. reesii showed growth on a limited range of carbohydrates, primarily basic plant sugars and cell wall components; this suggests that Onygenales, including dimorphic fungi, can degrade cellulosic plant material in the soil. In addition, U. reesii grew on gelatin and a wide range of dipeptides and amino acids, indicating a preference for proteinaceous growth substrates over carbohydrates, which may enable these fungi to also degrade animal biomass. These capabilities for degrading plant and animal substrates suggest a duality in lifestyle that could enable pathogenic species of Onygenales to transfer from soil to animal hosts.
ESTHER : Desjardins_2011_PLoS.Genet_7_e1002345
PubMedSearch : Desjardins_2011_PLoS.Genet_7_e1002345
PubMedID: 22046142
Gene_locus related to this paper: parbd-c1gc95 , parbp-c0s0d7 , parbp-c0s257 , parbd-c1g8z9 , parba-c1grf0 , parbp-c0s816 , parbp-c0s5g4 , parbd-c1g5f5 , parbd-c1fzf9 , parba-kex1 , parbd-kex1 , parbp-kex1 , parba-cbpya , parbp-cbpya

Title : Obligate biotrophy features unraveled by the genomic analysis of rust fungi - Duplessis_2011_Proc.Natl.Acad.Sci.U.S.A_108_9166
Author(s) : Duplessis S , Cuomo CA , Lin YC , Aerts A , Tisserant E , Veneault-Fourrey C , Joly DL , Hacquard S , Amselem J , Cantarel BL , Chiu R , Coutinho PM , Feau N , Field M , Frey P , Gelhaye E , Goldberg J , Grabherr MG , Kodira CD , Kohler A , Kues U , Lindquist EA , Lucas SM , Mago R , Mauceli E , Morin E , Murat C , Pangilinan JL , Park R , Pearson M , Quesneville H , Rouhier N , Sakthikumar S , Salamov AA , Schmutz J , Selles B , Shapiro H , Tanguay P , Tuskan GA , Henrissat B , Van de Peer Y , Rouze P , Ellis JG , Dodds PN , Schein JE , Zhong S , Hamelin RC , Grigoriev IV , Szabo LJ , Martin F
Ref : Proc Natl Acad Sci U S A , 108 :9166 , 2011
Abstract : Rust fungi are some of the most devastating pathogens of crop plants. They are obligate biotrophs, which extract nutrients only from living plant tissues and cannot grow apart from their hosts. Their lifestyle has slowed the dissection of molecular mechanisms underlying host invasion and avoidance or suppression of plant innate immunity. We sequenced the 101-Mb genome of Melampsora larici-populina, the causal agent of poplar leaf rust, and the 89-Mb genome of Puccinia graminis f. sp. tritici, the causal agent of wheat and barley stem rust. We then compared the 16,399 predicted proteins of M. larici-populina with the 17,773 predicted proteins of P. graminis f. sp tritici. Genomic features related to their obligate biotrophic lifestyle include expanded lineage-specific gene families, a large repertoire of effector-like small secreted proteins, impaired nitrogen and sulfur assimilation pathways, and expanded families of amino acid and oligopeptide membrane transporters. The dramatic up-regulation of transcripts coding for small secreted proteins, secreted hydrolytic enzymes, and transporters in planta suggests that they play a role in host infection and nutrient acquisition. Some of these genomic hallmarks are mirrored in the genomes of other microbial eukaryotes that have independently evolved to infect plants, indicating convergent adaptation to a biotrophic existence inside plant cells.
ESTHER : Duplessis_2011_Proc.Natl.Acad.Sci.U.S.A_108_9166
PubMedSearch : Duplessis_2011_Proc.Natl.Acad.Sci.U.S.A_108_9166
PubMedID: 21536894
Gene_locus related to this paper: pucgt-e3k840 , pucgt-e3kaq6 , pucgt-e3kw59 , pucgt-e3kz16 , pucgt-e3l9v6 , pucgt-e3l279 , pucgt-h6qt25 , mellp-f4reh4 , mellp-f4rhc8 , mellp-f4reh2 , mellp-f4r3y0 , mellp-f4rz15 , mellp-f4rz64 , mellp-f4rl14 , mellp-f4rz66 , mellp-f4s751 , mellp-f4s2g6 , pucgt-e3l1z7 , pucgt-e3l803 , pucgt-e3kst2 , pucgt-e3kst5 , mellp-f4ru03 , pucgt-e3l1z8 , pucgt-e3ktz7 , pucgt-e3jun4 , mellp-f4rl65 , mellp-f4rz16 , mellp-f4ru02 , mellp-f4sav4 , mellp-f4sav3 , mellp-f4s1j0 , mellp-f4rkp0 , mellp-f4s483 , pucgt-e3kzu5 , pucgt-h6qtq8 , mellp-f4r5l5 , pucgt-e3krw7 , pucgt-e3l7w5 , pucgt-e3k2w6 , pucgt-e3kfg2 , pucgt-kex1

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 : Evolution of pathogenicity and sexual reproduction in eight Candida genomes - Butler_2009_Nature_459_657
Author(s) : Butler G , Rasmussen MD , Lin MF , Santos MA , Sakthikumar S , Munro CA , Rheinbay E , Grabherr M , Forche A , Reedy JL , Agrafioti I , Arnaud MB , Bates S , Brown AJ , Brunke S , Costanzo MC , Fitzpatrick DA , de Groot PW , Harris D , Hoyer LL , Hube B , Klis FM , Kodira C , Lennard N , Logue ME , Martin R , Neiman AM , Nikolaou E , Quail MA , Quinn J , Santos MC , Schmitzberger FF , Sherlock G , Shah P , Silverstein KA , Skrzypek MS , Soll D , Staggs R , Stansfield I , Stumpf MP , Sudbery PE , Srikantha T , Zeng Q , Berman J , Berriman M , Heitman J , Gow NA , Lorenz MC , Birren BW , Kellis M , Cuomo CA
Ref : Nature , 459 :657 , 2009
Abstract : Candida species are the most common cause of opportunistic fungal infection worldwide. Here we report the genome sequences of six Candida species and compare these and related pathogens and non-pathogens. There are significant expansions of cell wall, secreted and transporter gene families in pathogenic species, suggesting adaptations associated with virulence. Large genomic tracts are homozygous in three diploid species, possibly resulting from recent recombination events. Surprisingly, key components of the mating and meiosis pathways are missing from several species. These include major differences at the mating-type loci (MTL); Lodderomyces elongisporus lacks MTL, and components of the a1/2 cell identity determinant were lost in other species, raising questions about how mating and cell types are controlled. Analysis of the CUG leucine-to-serine genetic-code change reveals that 99% of ancestral CUG codons were erased and new ones arose elsewhere. Lastly, we revise the Candida albicans gene catalogue, identifying many new genes.
ESTHER : Butler_2009_Nature_459_657
PubMedSearch : Butler_2009_Nature_459_657
PubMedID: 19465905
Gene_locus related to this paper: canal-ATG15 , canal-bna7 , canal-c4yl13 , canal-LIP1 , canal-LIP2 , canal-LIP3 , canal-LIP4 , canal-LIP5 , canal-LIP6 , canal-LIP7 , canal-LIP8 , canal-LIP9 , canal-LIP10 , canal-ppme1 , canal-q5a0c9 , canal-q5a2i9 , canal-q5a042 , canal-q5ad17 , canal-q5aeu3 , canal-q5afp8 , canal-q5ag57 , canal-q5ai09 , canal-q5ai12 , canal-q5ajt3 , canal-q5akz5 , canal-q5apu4 , canal-q59l46 , canal-q59m48 , canal-q59nw6 , canal-q59u61 , canal-q59u64 , canal-q59vp0 , canal-q59y97 , canaw-c4ykb1 , canaw-c4yrn6 , canaw-c4yrn9 , canaw-c4yrr3 , canaw-c4yrv3 , canaw-c4ys26 , cantt-c5m3d7 , cantt-c5m3y5 , cantt-c5m4x0 , cantt-c5m5e8 , cantt-c5m5w2 , cantt-c5m8s7 , cantt-c5m9c2 , cantt-c5m465 , cantt-c5m751 , cantt-c5m793 , cantt-c5m893 , cantt-c5ma78 , cantt-c5mag0 , cantt-c5mbb8 , cantt-c5mc53 , cantt-c5md87 , cantt-c5mdy3 , cantt-c5mey7 , cantt-c5mfg0 , cantt-c5mfh8 , cantt-c5mg56 , cantt-c5mgj0 , cantt-c5mh75 , cantt-c5mh80 , cantt-c5mh89 , cantt-c5mhh0 , cantt-c5mhn5 , cantt-c5mij5 , cantt-c5min7 , clal4-c4xvt8 , clal4-c4xwy4 , clal4-c4xy03 , clal4-c4xyx9 , clal4-c4xzz1 , clal4-c4y3e1 , clal4-c4y4f2 , clal4-c4y4w8 , clal4-c4y5j4 , clal4-c4y5j9 , clal4-c4y7z7 , clal4-c4y8q1 , clal4-c4y035 , clal4-c4y481 , clal4-c4y538 , clal4-c4y898 , clal4-c4yas2 , clal4-c4yba6 , clal4-c4yba7 , clal4-c4yc85 , lodel-a5drz3 , lodel-a5ds97 , lodel-a5dsc0 , lodel-a5duu4 , lodel-a5duy7 , lodel-a5dv03 , lodel-a5dv46 , lodel-a5dw16 , lodel-a5dwv7 , lodel-a5dww6 , lodel-a5dxf3 , lodel-a5e0z5 , lodel-a5e1c1 , lodel-a5e1l4 , lodel-a5e1p3 , lodel-a5e2s1 , lodel-a5e2t8 , lodel-a5e2v2 , lodel-a5e4u8 , lodel-a5e5a9 , lodel-a5e5k1 , lodel-a5e5z7 , lodel-a5e6w1 , lodel-a5e028 , lodel-atg15 , lodel-kex1 , picgu-a5d9u2 , picgu-a5dav0 , picgu-a5dbk0 , picgu-a5dc45 , picgu-a5dc73 , picgu-a5dc74 , picgu-a5dc75 , picgu-a5ddt8 , picgu-a5dev7 , picgu-a5dh90 , picgu-a5dhe3 , picgu-a5di38 , picgu-a5dj06 , picgu-a5dkd8 , picgu-a5dle9 , picgu-a5dlj5 , picgu-a5dm19 , picgu-a5dn92 , picgu-a5dnr3 , picgu-a5dnt6 , picgu-a5dqu5 , picgu-a5dr14 , picgu-a5drl3 , picgu-atg15 , picgu-bna7 , picgu-a5d9q3 , picgu-a5dag9 , clal4-c4y5a2 , clal4-c4y0l0 , cantt-c5mcb1 , clal4-c4y8j2 , cantt-c5m494 , clals-a0a202gac7 , canal-hda1 , picgu-a5dks8 , lodel-a5drs6 , canpc-g8bbk1 , cantt-kex1 , clal4-kex1 , picgu-kex1