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Complete genome sequence of Pseudomonas aeruginosa PAO1, an opportunistic pathogen 总被引:45,自引:0,他引:45
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 《Nature》2000,406(6799):959-964
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. 相似文献
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Frezza C Zheng L Folger O Rajagopalan KN MacKenzie ED Jerby L Micaroni M Chaneton B Adam J Hedley A Kalna G Tomlinson IP Pollard PJ Watson DG Deberardinis RJ Shlomi T Ruppin E Gottlieb E 《Nature》2011,477(7363):225-228
Fumarate hydratase (FH) is an enzyme of the tricarboxylic acid cycle (TCA cycle) that catalyses the hydration of fumarate into malate. Germline mutations of FH are responsible for hereditary leiomyomatosis and renal-cell cancer (HLRCC). It has previously been demonstrated that the absence of FH leads to the accumulation of fumarate, which activates hypoxia-inducible factors (HIFs) at normal oxygen tensions. However, so far no mechanism that explains the ability of cells to survive without a functional TCA cycle has been provided. Here we use newly characterized genetically modified kidney mouse cells in which Fh1 has been deleted, and apply a newly developed computer model of the metabolism of these cells to predict and experimentally validate a linear metabolic pathway beginning with glutamine uptake and ending with bilirubin excretion from Fh1-deficient cells. This pathway, which involves the biosynthesis and degradation of haem, enables Fh1-deficient cells to use the accumulated TCA cycle metabolites and permits partial mitochondrial NADH production. We predicted and confirmed that targeting this pathway would render Fh1-deficient cells non-viable, while sparing wild-type Fh1-containing cells. This work goes beyond identifying a metabolic pathway that is induced in Fh1-deficient cells to demonstrate that inhibition of haem oxygenation is synthetically lethal when combined with Fh1 deficiency, providing a new potential target for treating HLRCC patients. 相似文献
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用红外光谱法测定表明:各种硅胶负载仲进型铑催化剂上,线CO/桥CO红外吸收强度比值与金属助剂(M)的关系变化顺序为(50:1)(Rh-Mn)〉(22:1)(Rh-Li)〉(9.1:1)(Rh-Mn-Fe-Li)〉(3.5:1)(Rh-Fe)〉2.8:1)(Rh)。在各种Rh-M/SiO2催化剂上,线、桥CO吸附态的加氢原位FTIR跟踪实验表明:随着加氢的进行,线CO/桥CO吸收强度比值均逐渐减少… 相似文献
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