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Author Report for: Brinkman FS

Title: The genome sequence of taurine cattle: a window to ruminant biology and evolution
Elsik CG, Tellam RL, Worley KC, Gibbs RA, Muzny DM, Weinstock GM, Adelson DL, Eichler EE, Elnitski L and Zhao FQ <297 more author(s)> Elsik CG, Tellam RL, Worley KC, Gibbs RA, Muzny DM, Weinstock GM, Adelson DL, Eichler EE, Elnitski L, Guigo R, Hamernik DL, Kappes SM, Lewin HA, Lynn DJ, Nicholas FW, Reymond A, Rijnkels M, Skow LC, Zdobnov EM, Schook L, Womack J, Alioto T, Antonarakis SE, Astashyn A, Chapple CE, Chen HC, Chrast J, Camara F, Ermolaeva O, Henrichsen CN, Hlavina W, Kapustin Y, Kiryutin B, Kitts P, Kokocinski F, Landrum M, Maglott D, Pruitt K, Sapojnikov V, Searle SM, Solovyev V, Souvorov A, Ucla C, Wyss C, Anzola JM, Gerlach D, Elhaik E, Graur D, Reese JT, Edgar RC, McEwan JC, Payne GM, Raison JM, Junier T, Kriventseva EV, Eyras E, Plass M, Donthu R, Larkin DM, Reecy J, Yang MQ, Chen L, Cheng Z, Chitko-McKown CG, Liu GE, Matukumalli LK, Song J, Zhu B, Bradley DG, Brinkman FS, Lau LP, Whiteside MD, Walker A, Wheeler TT, Casey T, German JB, Lemay DG, Maqbool NJ, Molenaar AJ, Seo S, Stothard P, Baldwin CL, Baxter R, Brinkmeyer-Langford CL, Brown WC, Childers CP, Connelley T, Ellis SA, Fritz K, Glass EJ, Herzig CT, Iivanainen A, Lahmers KK, Bennett AK, Dickens CM, Gilbert JG, Hagen DE, Salih H, Aerts J, Caetano AR, Dalrymple B, Garcia JF, Gill CA, Hiendleder SG, Memili E, Spurlock D, Williams JL, Alexander L, Brownstein MJ, Guan L, Holt RA, Jones SJ, Marra MA, Moore R, Moore SS, Roberts A, Taniguchi M, Waterman RC, Chacko J, Chandrabose MM, Cree A, Dao MD, Dinh HH, Gabisi RA, Hines S, Hume J, Jhangiani SN, Joshi V, Kovar CL, Lewis LR, Liu YS, Lopez J, Morgan MB, Nguyen NB, Okwuonu GO, Ruiz SJ, Santibanez J, Wright RA, Buhay C, Ding Y, Dugan-Rocha S, Herdandez J, Holder M, Sabo A, Egan A, Goodell J, Wilczek-Boney K, Fowler GR, Hitchens ME, Lozado RJ, Moen C, Steffen D, Warren JT, Zhang J, Chiu R, Schein JE, Durbin KJ, Havlak P, Jiang H, Liu Y, Qin X, Ren Y, Shen Y, Song H, Bell SN, Davis C, Johnson AJ, Lee S, Nazareth LV, Patel BM, Pu LL, Vattathil S, Williams RL, Jr., Curry S, Hamilton C, Sodergren E, Wheeler DA, Barris W, Bennett GL, Eggen A, Green RD, Harhay GP, Hobbs M, Jann O, Keele JW, Kent MP, Lien S, McKay SD, McWilliam S, Ratnakumar A, Schnabel RD, Smith T, Snelling WM, Sonstegard TS, Stone RT, Sugimoto Y, Takasuga A, Taylor JF, Van Tassell CP, Macneil MD, Abatepaulo AR, Abbey CA, Ahola V, Almeida IG, Amadio AF, Anatriello E, Bahadue SM, Biase FH, Boldt CR, Carroll JA, Carvalho WA, Cervelatti EP, Chacko E, Chapin JE, Cheng Y, Choi J, Colley AJ, de Campos TA, De Donato M, Santos IK, de Oliveira CJ, Deobald H, Devinoy E, Donohue KE, Dovc P, Eberlein A, Fitzsimmons CJ, Franzin AM, Garcia GR, Genini S, Gladney CJ, Grant JR, Greaser ML, Green JA, Hadsell DL, Hakimov HA, Halgren R, Harrow JL, Hart EA, Hastings N, Hernandez M, Hu ZL, Ingham A, Iso-Touru T, Jamis C, Jensen K, Kapetis D, Kerr T, Khalil SS, Khatib H, Kolbehdari D, Kumar CG, Kumar D, Leach R, Lee JC, Li C, Logan KM, Malinverni R, Marques E, Martin WF, Martins NF, Maruyama SR, Mazza R, McLean KL, Medrano JF, Moreno BT, More DD, Muntean CT, Nandakumar HP, Nogueira MF, Olsaker I, Pant SD, Panzitta F, Pastor RC, Poli MA, Poslusny N, Rachagani S, Ranganathan S, Razpet A, Riggs PK, Rincon G, Rodriguez-Osorio N, Rodriguez-Zas SL, Romero NE, Rosenwald A, Sando L, Schmutz SM, Shen L, Sherman L, Southey BR, Lutzow YS, Sweedler JV, Tammen I, Telugu BP, Urbanski JM, Utsunomiya YT, Verschoor CP, Waardenberg AJ, Wang Z, Ward R, Weikard R, Welsh TH, Jr., White SN, Wilming LG, Wunderlich KR, Yang J, Zhao FQ (- 297)
Ref: Science, 324:522, 2009 : PubMed
Abstract


ESTHER: Elsik_2009_Science_324_522
PubMedSearch: Elsik 2009 Science 324 522
PubMedID: 19390049
Gene_locus related to this paper: bovin-2neur, bovin-a0jnh8, bovin-a5d7b7, bovin-ACHE, bovin-balip, bovin-dpp4, bovin-dpp6, bovin-e1bi31, bovin-e1bn79, bovin-est8, bovin-f1mbd6, bovin-f1mi11, bovin-f1mr65, bovin-f1n1l4, bovin-g3mxp5, bovin-q0vcc8, bovin-q2kj30, bovin-q3t0r6, bovin-thyro

Abstract

To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.



        

Title: Newly introduced genomic prophage islands are critical determinants of in vivo competitiveness in the Liverpool Epidemic Strain of Pseudomonas aeruginosa
Winstanley C, Langille MG, Fothergill JL, Kukavica-Ibrulj I, Paradis-Bleau C, Sanschagrin F, Thomson NR, Winsor GL, Quail MA and Levesque RC <9 more author(s)> Winstanley C, Langille MG, Fothergill JL, Kukavica-Ibrulj I, Paradis-Bleau C, Sanschagrin F, Thomson NR, Winsor GL, Quail MA, Lennard N, Bignell A, Clarke L, Seeger K, Saunders D, Harris D, Parkhill J, Hancock RE, Brinkman FS, Levesque RC (- 9)
Ref: Genome Res, 19:12, 2009 : PubMed
Abstract


ESTHER: Winstanley_2009_Genome.Res_19_12
PubMedSearch: Winstanley 2009 Genome.Res 19 12
PubMedID: 19047519
Gene_locus related to this paper: pseae-clipa, pseae-CPO, pseae-llipa, pseae-metx, pseae-PA0201, pseae-PA0231, pseae-PA0308, pseae-PA0368, pseae-PA0480, pseae-PA0502, pseae-PA0543, pseae-PA0599, pseae-PA1166, pseae-PA1291, pseae-PA1304, pseae-PA1510, pseae-PA1558, pseae-PA1597, pseae-PA1907, pseae-PA2086, pseae-PA2098, pseae-PA2302, pseae-PA2425, pseae-PA2451, pseae-PA2540, pseae-PA2682, pseae-PA2689, pseae-PA2745, pseae-PA2764, pseae-PA2927, pseae-PA2934, pseae-PA2949, pseae-PA3132, pseae-PA3301, pseae-PA3324, pseae-PA3327, pseae-PA3429, pseae-PA3586, pseae-PA3628, pseae-PA3695, pseae-PA3859, pseae-PA3994, pseae-PA4152, pseae-PA4968, pseae-PA5080, pseae-PCHC, pseae-PCHF, pseae-PHAC2, pseae-phaD, pseae-phag, pseae-Q9APW4, pseae-rhla, pseae-q9i252

Abstract

Pseudomonas aeruginosa isolates have a highly conserved core genome representing up to 90% of the total genomic sequence with additional variable accessory genes, many of which are found in genomic islands or islets. The identification of the Liverpool Epidemic Strain (LES) in a children's cystic fibrosis (CF) unit in 1996 and its subsequent observation in several centers in the United Kingdom challenged the previous widespread assumption that CF patients acquire only unique strains of P. aeruginosa from the environment. To learn about the forces that shaped the development of this important epidemic strain, the genome of the earliest archived LES isolate, LESB58, was sequenced. The sequence revealed the presence of many large genomic islands, including five prophage clusters, one defective (pyocin) prophage cluster, and five non-phage islands. To determine the role of these clusters, an unbiased signature tagged mutagenesis study was performed, followed by selection in the chronic rat lung infection model. Forty-seven mutants were identified by sequencing, including mutants in several genes known to be involved in Pseudomonas infection. Furthermore, genes from four prophage clusters and one genomic island were identified and in direct competition studies with the parent isolate; four were demonstrated to strongly impact on competitiveness in the chronic rat lung infection model. This strongly indicates that enhanced in vivo competitiveness is a major driver for maintenance and diversifying selection of these genomic prophage genes.



        

Title: The complete genome of Rhodococcus sp. RHA1 provides insights into a catabolic powerhouse
McLeod MP, Warren RL, Hsiao WW, Araki N, Myhre M, Fernandes C, Miyazawa D, Wong W, Lillquist AL and Eltis LD <19 more author(s)> McLeod MP, Warren RL, Hsiao WW, Araki N, Myhre M, Fernandes C, Miyazawa D, Wong W, Lillquist AL, Wang D, Dosanjh M, Hara H, Petrescu A, Morin RD, Yang G, Stott JM, Schein JE, Shin H, Smailus D, Siddiqui AS, Marra MA, Jones SJ, Holt R, Brinkman FS, Miyauchi K, Fukuda M, Davies JE, Mohn WW, Eltis LD (- 19)
Ref: Proc Natl Acad Sci U S A, 103:15582, 2006 : PubMed
Abstract


ESTHER: McLeod_2006_Proc.Natl.Acad.Sci.U.S.A_103_15582
PubMedSearch: McLeod 2006 Proc.Natl.Acad.Sci.U.S.A 103 15582
PubMedID: 17030794
Gene_locus related to this paper: rhoob-c1ar27, rhoob-c1arb5, rhoob-c1asz4, rhoob-c1at13, rhoob-c1ata3, rhoob-c1atk8, rhoob-c1atq0, rhoob-c1ats8, rhoob-c1att5, rhoob-c1au11, rhoob-c1auh5, rhoob-c1aux1, rhoob-c1av24, rhoob-c1awr1, rhoob-c1axf2, rhoob-c1ayb0, rhoob-c1b0a8, rhoob-c1b0g7, rhoob-c1b0w8, rhoob-c1b1i6, rhoob-c1b7t4, rhoob-c1b8z9, rhoob-c1b9l2, rhoob-c1b9v1, rhoob-c1b9y1, rhoob-c1b930, rhoob-c1b931, rhoob-c1b932, rhoob-c1b996, rhoob-c1bbl3, rhoob-c1bbq4, rhoop-pcaL, rhosp-bphD2, rhosp-EtbD1, rhosr-q0rwt2, rhosr-q0rwv3, rhosr-q0rxc8, rhosr-q0ryc0, rhosr-q0ryn3, rhosr-q0rz46, rhosr-q0rz78, rhosr-q0s0s0, rhosr-q0s1l0, rhosr-q0s1m1, rhosr-q0s1n4, rhosr-q0s1x5, rhosr-q0s1x6, rhosr-q0s2i6, rhosr-q0s2n9, rhosr-q0s2t5, rhosr-q0s3c8, rhosr-q0s3s6, rhosr-q0s4f1, rhosr-q0s5h5, rhosr-q0s5m7, rhosr-q0s6a9, rhosr-q0s6b3, rhosr-q0s6b5, rhosr-q0s7i7, rhosr-q0s7r1, rhosr-q0s008, rhosr-q0s8b3, rhosr-q0s8f4, rhosr-q0s8p7, rhosr-q0s8z9, rhosr-q0s9l3, rhosr-q0s9m1, rhosr-q0s101, rhosr-q0s125, rhosr-q0s230, rhosr-q0s252, rhosr-q0s393, rhosr-q0s477, rhosr-q0s545, rhojr-q0s546, rhosr-q0s837, rhosr-q0s849, rhosr-q0sa25, rhosr-q0sa26, rhosr-q0sa61, rhosr-q0saa5, rhosr-q0san0, rhosr-q0saw3, rhosr-q0sbd3, rhosr-q0sc04, rhosr-q0scq2, rhosr-q0sd10, rhosr-q0sdb8, rhosr-q0sdh6, rhosr-q0sdr2, rhosr-q0sdr5, rhosr-q0sdt1, rhosr-q0sdu5, rhosr-q0sej4, rhosr-q0ses6, rhosr-q0set7, rhosr-q0sex8, rhosr-q0sf05, rhosr-q0sfh8, rhosr-q0sfl2, rhosr-q0sfz6, rhosr-q0sgc8, rhosr-q0sgj4, rhosr-q0sgv4, rhosr-q0sgw4, rhosr-q0sh74, rhosr-q0shd6, rhosr-q0shi2, rhosr-q0sjy0, rhosr-q0skn1, rhoob-c1b934, rhosr-q0sab7, rhosr-q0rwx4, rhoob-c1asm3, rhosr-q0ruu2, rhosr-q0s747, rhosr-q0ry47, rhosr-q0rwa1, rhosr-q0sj22, 9noca-j2j8s8, rhojr-q0sd80, rhojr-q0sf05

Abstract

Rhodococcus sp. RHA1 (RHA1) is a potent polychlorinated biphenyl-degrading soil actinomycete that catabolizes a wide range of compounds and represents a genus of considerable industrial interest. RHA1 has one of the largest bacterial genomes sequenced to date, comprising 9,702,737 bp (67% G+C) arranged in a linear chromosome and three linear plasmids. A targeted insertion methodology was developed to determine the telomeric sequences. RHA1's 9,145 predicted protein-encoding genes are exceptionally rich in oxygenases (203) and ligases (192). Many of the oxygenases occur in the numerous pathways predicted to degrade aromatic compounds (30) or steroids (4). RHA1 also contains 24 nonribosomal peptide synthase genes, six of which exceed 25 kbp, and seven polyketide synthase genes, providing evidence that rhodococci harbor an extensive secondary metabolism. Among sequenced genomes, RHA1 is most similar to those of nocardial and mycobacterial strains. The genome contains few recent gene duplications. Moreover, three different analyses indicate that RHA1 has acquired fewer genes by recent horizontal transfer than most bacteria characterized to date and far fewer than Burkholderia xenovorans LB400, whose genome size and catabolic versatility rival those of RHA1. RHA1 and LB400 thus appear to demonstrate that ecologically similar bacteria can evolve large genomes by different means. Overall, RHA1 appears to have evolved to simultaneously catabolize a diverse range of plant-derived compounds in an O(2)-rich environment. In addition to establishing RHA1 as an important model for studying actinomycete physiology, this study provides critical insights that facilitate the exploitation of these industrially important microorganisms.



        

Title: Complete genome sequence of Pseudomonas aeruginosa PAO1, an opportunistic pathogen
Stover CK, Pham XQ, Erwin AL, Mizoguchi SD, Warrener P, Hickey MJ, Brinkman FS, Hufnagle WO, Kowalik DJ and Olson MV <21 more author(s)> Stover CK, Pham XQ, Erwin AL, Mizoguchi SD, Warrener P, Hickey MJ, Brinkman FS, Hufnagle WO, Kowalik DJ, Lagrou M, Garber RL, Goltry L, Tolentino E, Westbrock-Wadman S, Yuan Y, Brody LL, Coulter SN, Folger KR, Kas A, Larbig K, Lim R, Smith K, Spencer D, Wong GK, Wu Z, Paulsen IT, Reizer J, Saier MH, Hancock RE, Lory S, Olson MV (- 21)
Ref: Nature, 406:959, 2000 : PubMed
Abstract


ESTHER: Stover_2000_Nature_406_959
PubMedSearch: Stover 2000 Nature 406 959
PubMedID: 10984043
Gene_locus related to this paper: pseae-clipa, pseae-CPO, pseae-metx, pseae-PA0201, pseae-PA0231, pseae-PA0308, pseae-PA0368, pseae-PA0480, pseae-PA0502, pseae-PA0543, pseae-PA0599, pseae-PA0829, pseae-PA1166, pseae-PA1211, pseae-PA1239, pseae-PA1291, pseae-PA1304, pseae-PA1510, pseae-PA1558, pseae-PA1597, pseae-PA1621, pseae-PA1622, pseae-PA1680, pseae-PA1771, pseae-PA1888, pseae-PA1907, pseae-PA1990, pseae-PA2086, pseae-PA2098, pseae-PA2168, pseae-PA2302, pseae-PA2411, pseae-PA2425, pseae-PA2451, pseae-PA2540, pseae-PA2682, pseae-PA2689, pseae-PA2745, pseae-PA2764, pseae-PA2927, pseae-PA2934, pseae-PA2949, pseae-PA3053, pseae-PA3132, pseae-PA3226, pseae-PA3301, pseae-PA3324, pseae-PA3327, pseae-PA3429, pseae-PA3509, pseae-PA3586, pseae-PA3628, pseae-PA3695, pseae-PA3734, pseae-PA3829, pseae-PA3859, pseae-PA3994, pseae-PA4008, pseae-PA4152, pseae-PA4440, pseae-PA4968, pseae-PA5080, pseae-PA5384, pseae-PA5513, pseae-PCHC, pseae-PCHF, pseae-PHAC1, pseae-PHAC2, pseae-phaD, pseae-phag, pseae-PVDD, pseae-q9i4b9, pseae-q9i538, pseae-rhla, pseae-Y2218, pseae-q9hyv3, pseae-q9i252, pseae-q9i6m9

Abstract

Pseudomonas aeruginosa is a ubiquitous environmental bacterium that is one of the top three causes of opportunistic human infections. A major factor in its prominence as a pathogen is its intrinsic resistance to antibiotics and disinfectants. Here we report the complete sequence of P. aeruginosa strain PAO1. At 6.3 million base pairs, this is the largest bacterial genome sequenced, and the sequence provides insights into the basis of the versatility and intrinsic drug resistance of P. aeruginosa. Consistent with its larger genome size and environmental adaptability, P. aeruginosa contains the highest proportion of regulatory genes observed for a bacterial genome and a large number of genes involved in the catabolism, transport and efflux of organic compounds as well as four potential chemotaxis systems. We propose that the size and complexity of the P. aeruginosa genome reflect an evolutionary adaptation permitting it to thrive in diverse environments and resist the effects of a variety of antimicrobial substances.



        

Title: Influence of a putative ECF sigma factor on expression of the major outer membrane protein, OprF, in Pseudomonas aeruginosa and Pseudomonas fluorescens
Brinkman FS, Schoofs G, Hancock RE, De Mot R
Ref: Journal of Bacteriology, 181:4746, 1999 : PubMed
Abstract


ESTHER: Brinkman_1999_J.Bacteriol_181_4746
PubMedSearch: Brinkman 1999 J.Bacteriol 181 4746
PubMedID: 10438740
Gene_locus related to this paper: psefl-EstX

Abstract

The gene encoding OprF, a major outer membrane protein in Pseudomonas species (formerly known as type 1 pseudomonads), was thought to be constitutively transcribed from a single sigma 70 promoter immediately upstream of the gene. We now report the identification of a novel putative ECF (extracytoplasmic function) sigma factor gene, sigX, located immediately upstream of oprF in both Pseudomonas aeruginosa PAO1 and Pseudomonas fluorescens OE 28.3 and show that disruption of this gene significantly reduces OprF expression. In P. aeruginosa, Northern analysis demonstrated that this reduction was a result of an effect on transcription of monocistronic oprF combined with a polar effect due to termination of a transcript containing sigX and oprF. Comparison of sigX-disrupted and wild-type cell transcripts by primer extension indicated that monocistronic transcription of oprF occurs from two overlapping promoters, one that is SigX-dependent and resembles ECF sigma factor promoters in its minus-35 region and another promoter that is independent of SigX and is analogous to the sigma 70-type promoter previously reported. Complementation of the P. aeruginosa sigX-disrupted mutant with plasmid-encoded OprF did not resolve the phenotypes associated with this mutant, which included a markedly reduced logarithmic-phase growth rate in rich medium (compared to that in minimal medium), further reduction of the growth rate in a low-osmolarity environment, secretion of an unidentified pigment, and increased sensitivity to the antibiotic imipenem. This indicates that SigX is involved in the regulation of other genes in P. aeruginosa. Disruption of the sigX gene in P. fluorescens also had an effect on the logarithmic-phase growth rate in rich medium. A conserved sigX gene was also identified in a Pseudomonas syringae isolate and six P. aeruginosa clinical isolates. Collectively, these data indicate that an ECF sigma factor plays a role in the regulation and expression of OprF and also affects other genes.