Author Report for: Malavazi INo contact information in database for Malavazi I
de Vries RP, Riley R, Wiebenga A, Aguilar-Osorio G, Amillis S, Uchima CA, Anderluh G, Asadollahi M, Askin M and Grigoriev IV <107 more author(s)> de Vries RP, Riley R, Wiebenga A, Aguilar-Osorio G, Amillis S, Uchima CA, Anderluh G, Asadollahi M, Askin M, Barry K, Battaglia E, Bayram O, Benocci T, Braus-Stromeyer SA, Caldana C, Canovas D, Cerqueira GC, Chen F, Chen W, Choi C, Clum A, Dos Santos RA, Damasio AR, Diallinas G, Emri T, Fekete E, Flipphi M, Freyberg S, Gallo A, Gournas C, Habgood R, Hainaut M, Harispe ML, Henrissat B, Hilden KS, Hope R, Hossain A, Karabika E, Karaffa L, Karanyi Z, Krasevec N, Kuo A, Kusch H, LaButti K, Lagendijk EL, Lapidus A, Levasseur A, Lindquist E, Lipzen A, Logrieco AF, Maccabe A, Makela MR, Malavazi I, Melin P, Meyer V, Mielnichuk N, Miskei M, Molnar AP, Mule G, Ngan CY, Orejas M, Orosz E, Ouedraogo JP, Overkamp KM, Park HS, Perrone G, Piumi F, Punt PJ, Ram AF, Ramon A, Rauscher S, Record E, Riano-Pachon DM, Robert V, Rohrig J, Ruller R, Salamov A, Salih NS, Samson RA, Sandor E, Sanguinetti M, Schutze T, Sepcic K, Shelest E, Sherlock G, Sophianopoulou V, Squina FM, Sun H, Susca A, Todd RB, Tsang A, Unkles SE, van de Wiele N, van Rossen-Uffink D, Oliveira JV, Vesth TC, Visser J, Yu JH, Zhou M, Andersen MR, Archer DB, Baker SE, Benoit I, Brakhage AA, Braus GH, Fischer R, Frisvad JC, Goldman GH, Houbraken J, Oakley B, Pocsi I, Scazzocchio C, Seiboth B, vanKuyk PA, Wortman J, Dyer PS, Grigoriev IV (- 107) Ref: Genome Biol, 18:28, 2017 : PubMed ESTHER: de Vries_2017_Genome.Biol_18_28 PubMedSearch: de Vries 2017 Genome.Biol 18 28 PubMedID: 28196534 Gene_locus related to this paper: asptu-a0a1l9nhd0, aspve-a0a1l9pxx8, aspve-a0a1l9q4m3, aspwe-a0a1l9s133, 9euro-a0a1l9t3v9, aspwe-a0a1l9rcx6, aspna-g3y5a6, aspgl-a0a1l9v4d3, 9euro-a0a1l9sa36, aspsb-a0a319eji6, aspve-a0a1l9px96, 9euro-a0a1l9tay1, aspgl-a0a1l9vbc0, aspc5-a0a1r3rh65, 9euro-a0a2v5i956, aspwe-a0a1l9rpp6, aspna-g3xpw9, aspve-a0a1l9plv1, 9euro-a0a1l9tk47, aspve-a0a1l9pde9, aspve-a0a1l9pz72, aspwe-a0a1l9rde6, 9euro-a0a1l9tdb5, aspkw-g7xq95, aspbc-a0a1l9u6h4, aspbc-a0a1l9u2l4, asptc-a0a1l9mx83, aspgl-a0a1l9ve90, aspve-a0a1l9pvz9, 9euro-a0a1l9tdh3, aspc5-a0a1r3rmn9, aspwe-a0a1l9rlq2, asptc-a0a1l9nby7, aspng-a0a100i8t9, aspc5-a0a1r3rem6, aspbc-a0a1l9uy89, aspa1-anee, aspa1-aneh, aspa1-acrc, aspbc-alba, aspa1-acui Abstract BACKGROUND: The fungal genus Aspergillus is of critical importance to humankind. Species include those with industrial applications, important pathogens of humans, animals and crops, a source of potent carcinogenic contaminants of food, and an important genetic model. The genome sequences of eight aspergilli have already been explored to investigate aspects of fungal biology, raising questions about evolution and specialization within this genus. RESULTS: We have generated genome sequences for ten novel, highly diverse Aspergillus species and compared these in detail to sister and more distant genera. Comparative studies of key aspects of fungal biology, including primary and secondary metabolism, stress response, biomass degradation, and signal transduction, revealed both conservation and diversity among the species. Observed genomic differences were validated with experimental studies. This revealed several highlights, such as the potential for sex in asexual species, organic acid production genes being a key feature of black aspergilli, alternative approaches for degrading plant biomass, and indications for the genetic basis of stress response. A genome-wide phylogenetic analysis demonstrated in detail the relationship of the newly genome sequenced species with other aspergilli. CONCLUSIONS: Many aspects of biological differences between fungal species cannot be explained by current knowledge obtained from genome sequences. The comparative genomics and experimental study, presented here, allows for the first time a genus-wide view of the biological diversity of the aspergilli and in many, but not all, cases linked genome differences to phenotype. Insights gained could be exploited for biotechnological and medical applications of fungi. Title: Comparative genomic analysis of human fungal pathogens causing paracoccidioidomycosis Desjardins CA, Champion MD, Holder JW, Muszewska A, Goldberg J, Bailao AM, Brigido MM, Ferreira ME, Garcia AM and Cuomo CA <32 more 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 (- 32) Ref: PLoS Genet, 7:e1002345, 2011 : PubMed 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 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. Title: Genomic islands in the pathogenic filamentous fungus Aspergillus fumigatus Fedorova ND, Khaldi N, Joardar VS, Maiti R, Amedeo P, Anderson MJ, Crabtree J, Silva JC, Badger JH and Nierman WC <29 more author(s)> Fedorova ND, Khaldi N, Joardar VS, Maiti R, Amedeo P, Anderson MJ, Crabtree J, Silva JC, Badger JH, Albarraq A, Angiuoli S, Bussey H, Bowyer P, Cotty PJ, Dyer PS, Egan A, Galens K, Fraser-Liggett CM, Haas BJ, Inman JM, Kent R, Lemieux S, Malavazi I, Orvis J, Roemer T, Ronning CM, Sundaram JP, Sutton G, Turner G, Venter JC, White OR, Whitty BR, Youngman P, Wolfe KH, Goldman GH, Wortman JR, Jiang B, Denning DW, Nierman WC (- 29) Ref: PLoS Genet, 4:e1000046, 2008 : PubMed ESTHER: Fedorova_2008_PLoS.Genet_4_E1000046 PubMedSearch: Fedorova 2008 PLoS.Genet 4 E1000046 PubMedID: 18404212 Gene_locus related to this paper: aspcl-a1c4m6, aspcl-a1c5a7, aspcl-a1c6w3, aspcl-a1c8p7, aspcl-a1c8q9, aspcl-a1c9k4, aspcl-a1c759, aspcl-a1c786, aspcl-a1c823, aspcl-a1c859, aspcl-a1c881, aspcl-a1c994, aspcl-a1cag4, aspcl-a1caj8, aspcl-a1cas0, aspcl-a1cc86, aspcl-a1ccq2, aspcl-a1cfv7, aspcl-a1chj6, aspcl-a1cif4, aspcl-a1ck14, aspcl-a1cke4, aspcl-a1ckq1, aspcl-a1cli1, aspcl-a1cln8, aspcl-a1cm72, aspcl-a1cns2, aspcl-a1cpk9, aspcl-a1cra8, aspcl-a1crr5, aspcl-a1crs9, aspcl-a1cs04, aspcl-a1cs39, aspcl-a1cu39, aspcl-atg15, aspcl-axe1, aspcl-cuti1, aspcl-cuti3, aspcl-dapb, aspcl-dpp4, aspcl-dpp5, aspcl-faeb, aspcl-faec1, aspcl-faec2, aspfc-b0xp50, aspfc-b0xu40, aspfc-b0xzj6, aspfc-b0y2h6, aspfc-b0y962, aspfc-b0yaj6, aspfc-dpp5, aspfu-DPP4, aspfu-faeb1, aspfu-faec, aspfu-ppme1, aspfu-q4w9r3, aspfu-q4w9t5, aspfu-q4w9z4, aspfu-q4wa57, aspfu-q4wa78, aspfu-q4wag0, aspfu-q4wal3, aspfu-q4wbc5, aspfu-q4wbj7, aspfu-q4wdg2, aspfu-q4wf06, aspfu-q4wf29, aspfu-q4wf56, aspfu-q4wfq9, aspfu-q4wg73, aspfu-q4wgm4, aspfu-q4win2, aspfu-q4wk31, aspfu-q4wk44, aspfu-q4wk90, aspfu-q4wm12, aspfu-q4wm84, aspfu-q4wm86, aspfu-q4wmr0, aspfu-q4wny7, aspfu-q4wp19, aspfu-q4wpb9, aspfu-q4wqj8, aspfu-q4wqv2, aspfu-q4wrr7, aspfu-q4wu51, aspfu-q4wub2, aspfu-q4wui7, aspfu-q4wuk8, aspfu-q4wum3, aspfu-q4wuw0, aspfu-q4wvy1, aspfu-q4ww22, aspfu-q4wx13, aspfu-q4wxd0, aspfu-q4wxe4, aspfu-q4wxr1, aspfu-q4wyq5, aspfu-q4wz16, aspfu-q4wzd5, aspfu-q4wzh6, aspfu-q4x0n6, aspfu-q4x1n0, aspfu-q4x1w9, aspfu-q4x078, neofi-a1cwa6, neofi-a1d4m8, neofi-a1d4p0, neofi-a1d5p2, neofi-a1d104, neofi-a1d380, neofi-a1d512, neofi-a1d654, neofi-a1da18, neofi-a1dal8, neofi-a1df46, neofi-a1dhj0, neofi-a1di44, neofi-a1dk35, neofi-a1dki7, neofi-a1dkt6, neofi-a1dn55, neofi-atg15, neofi-axe1, neofi-faeb1, neofi-faeb2, neofi-faec, aspcl-a1cd34, aspcl-a1cd88, neofi-a1dc66, aspcl-a1ceh5, neofi-a1dfr9, aspfm-a0a084bf80, aspcl-a1cqb5, aspcl-a1cs44, neofi-a1d517, neofi-a1dbz0, neofi-a1cuz0, aspcl-a1c5e8, neofi-a1d0b8, aspcl-a1cdf0, aspcl-a1ccd3, neofi-a1da82, neofi-a1d5e6, aspcl-kex1, aspcl-cbpya Abstract We present the genome sequences of a new clinical isolate of the important human pathogen, Aspergillus fumigatus, A1163, and two closely related but rarely pathogenic species, Neosartorya fischeri NRRL181 and Aspergillus clavatus NRRL1. Comparative genomic analysis of A1163 with the recently sequenced A. fumigatus isolate Af293 has identified core, variable and up to 2% unique genes in each genome. While the core genes are 99.8% identical at the nucleotide level, identity for variable genes can be as low 40%. The most divergent loci appear to contain heterokaryon incompatibility (het) genes associated with fungal programmed cell death such as developmental regulator rosA. Cross-species comparison has revealed that 8.5%, 13.5% and 12.6%, respectively, of A. fumigatus, N. fischeri and A. clavatus genes are species-specific. These genes are significantly smaller in size than core genes, contain fewer exons and exhibit a subtelomeric bias. Most of them cluster together in 13 chromosomal islands, which are enriched for pseudogenes, transposons and other repetitive elements. At least 20% of A. fumigatus-specific genes appear to be functional and involved in carbohydrate and chitin catabolism, transport, detoxification, secondary metabolism and other functions that may facilitate the adaptation to heterogeneous environments such as soil or a mammalian host. Contrary to what was suggested previously, their origin cannot be attributed to horizontal gene transfer (HGT), but instead is likely to involve duplication, diversification and differential gene loss (DDL). The role of duplication in the origin of lineage-specific genes is further underlined by the discovery of genomic islands that seem to function as designated "gene dumps" and, perhaps, simultaneously, as "gene factories". | |||||||
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