Kuroda M

References (14)

Title : A girl with infantile neuronal ceroid lipofuscinosis caused by novel PPT1 mutation and paternal uniparental isodisomy of chromosome 1 - Niida_2016_Brain.Dev_38_674
Author(s) : Niida Y , Yokoi A , Kuroda M , Mitani Y , Nakagawa H , Ozaki M
Ref : Brain Dev , 38 :674 , 2016
Abstract : BACKGROUND: Infantile neuronal ceroid lipofuscinosis (INCL) is an autosomal recessive disorder starting in infancy as early as 12-month-old, caused by PPT1 (palmitoyl-protein thioesterase 1) mutations, and characterized by progressive psychomotor deterioration, brain atrophy, myoclonic jerk and visual impairment. INCL can be diagnosed by brain magnetic resonance image (MRI) prior to rapid deterioration stage. To date, there is no INCL patient whose manifestation was caused by uniparental isodisomy (UPiD). PATIENT: We reported a girl diagnosed with INCL. Genetic analysis revealed a novel PPT1 mutation c.20_47del28:p.Leu7Hisfs*21. Only the father of the patient was found as a carrier of this mutation. SNP array showed the mutation became homozygous by paternal UPiD of chromosome 1. DISCUSSION: Although ICNL is a rare disease except in Finland, it is not difficult to diagnose it since the clinical symptoms and MRI findings are characteristic. Genetic testing is useful for definitive diagnosis, and distinction of UPiD is essential for genetic counseling.
ESTHER : Niida_2016_Brain.Dev_38_674
PubMedSearch : Niida_2016_Brain.Dev_38_674
PubMedID: 26846731
Gene_locus related to this paper: human-PPT1

Title : A case of acquired lecithin:cholesterol acyltransferase deficiency with sarcoidosis that remitted spontaneously - Akiko_2016_CEN.Case.Rep_5_192
Author(s) : Akiko T , Okura T , Nagao T , Kukida M , Enomoto D , Miyoshi KI , Higaki J , Kuroda M , Bujo H
Ref : CEN Case Rep , 5 :192 , 2016
Abstract : Familial lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare inherited disorder that causes an extremely low high-density lipoprotein cholesterol concentration in serum. Recently, acquired LCAT deficiency caused by IgG antibodies to LCAT, without any LCAT gene mutation, was reported. Here we describe a case of acquired LCAT deficiency occurring in association with sarcoidosis. The patient was a Japanese female aged 70 years, had no mutation in the LCAT gene exon sequence, but had an LCAT inhibitor factor in her serum, detected using lipoprotein-deficient serum. She was diagnosed with acquired LCAT deficiency. Her abnormalities of serum lipoproteins improved spontaneously during three and a half years. Because they require different treatment strategies, distinction between familial lecithin:cholesterol acyltransferase deficiency (FLD) and acquired LCAT deficiency by gene sequencing is warranted, especially in cases without corneal clouding.
ESTHER : Akiko_2016_CEN.Case.Rep_5_192
PubMedSearch : Akiko_2016_CEN.Case.Rep_5_192
PubMedID: 28508975
Gene_locus related to this paper: human-LCAT

Title : Lipoprotein subfractions highly associated with renal damage in familial lecithin:cholesterol acyltransferase deficiency - Kuroda_2014_Arterioscler.Thromb.Vasc.Biol_34_1756
Author(s) : Kuroda M , Holleboom AG , Stroes ES , Asada S , Aoyagi Y , Kamata K , Yamashita S , Ishibashi S , Saito Y , Bujo H
Ref : Arterioscler Thromb Vasc Biol , 34 :1756 , 2014
Abstract : OBJECTIVE: In familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD), deposition of abnormal lipoproteins in the renal stroma ultimately leads to renal failure. However, fish-eye disease (FED) does not lead to renal damage although the causative mutations for both FLD and FED lie within the same LCAT gene. This study was performed to identify the lipoproteins important for the development of renal failure in genetically diagnosed FLD in comparison with FED, using high-performance liquid chromatography with a gel filtration column. APPROACH AND
RESULTS: Lipoprotein profiles of 9 patients with LCAT deficiency were examined. Four lipoprotein fractions specific to both FLD and FED were identified: (1) large lipoproteins (>80 nm), (2) lipoproteins corresponding to large low-density lipoprotein (LDL), (3) lipoproteins corresponding to small LDL to large high-density lipoprotein, and (4) to small high-density lipoprotein. Contents of cholesteryl ester and triglyceride of the large LDL in FLD (below detection limit and 45.8+/-3.8%) and FED (20.7+/-6.4% and 28.0+/-6.5%) were significantly different, respectively. On in vitro incubation with recombinant LCAT, content of cholesteryl ester in the large LDL in FLD, but not in FED, was significantly increased (to 4.2+/-1.4%), whereas dysfunctional high-density lipoprotein was diminished in both FLD and FED.
CONCLUSIONS: Our novel analytic approach using high-performance liquid chromatography with a gel filtration column identified large LDL and high-density lipoprotein with a composition specific to FLD, but not to FED. The abnormal lipoproteins were sensitive to treatment with recombinant LCAT and thus may play a causal role in the renal pathology of FLD.
ESTHER : Kuroda_2014_Arterioscler.Thromb.Vasc.Biol_34_1756
PubMedSearch : Kuroda_2014_Arterioscler.Thromb.Vasc.Biol_34_1756
PubMedID: 24876348
Gene_locus related to this paper: human-LCAT

Title : Amelioration of circulating lipoprotein profile and proteinuria in a patient with LCAT deficiency due to a novel mutation (Cys74Tyr) in the lid region of LCAT under a fat-restricted diet and ARB treatment - Naito_2013_Atherosclerosis_228_193
Author(s) : Naito S , Kamata M , Furuya M , Hayashi M , Kuroda M , Bujo H , Kamata K
Ref : Atherosclerosis , 228 :193 , 2013
Abstract : Familial lecithin-cholesterol acyltransferase (LCAT) deficiency is a hereditary disease characterized by an abnormal lipid profile, corneal opacity, anemia and progressive renal disease. We report a patient with complete loss of LCAT activity due to a novel lcat gene mutation of Cys74Tyr in the lid region of LCAT protein. Esterification of cholesterol in this patient was disturbed by disruption of a substrate binding loop of Cys50-Cys74 in LCAT protein. She had progressive renal dysfunction, proteinuria, corneal opacity, anemia and an abnormal lipid profile. Her serum lipids showed a significant increase in abnormal lipoproteins at the original position in agarose gel electrophoresis and VLDL-cholesterol, and a severe decrease in serum HDL-cholesterol. Lipoprotein analyzes also revealed the presence of an abnormal midband lipoprotein, and a maturation disturbance of HDL particles. Renal function and proteinuria improved following the adoption of a fat-restricted diet and administration of an angiotensin II receptor blocker. The abnormal lipoproteins also decreased after this treatment.
ESTHER : Naito_2013_Atherosclerosis_228_193
PubMedSearch : Naito_2013_Atherosclerosis_228_193
PubMedID: 23522979
Gene_locus related to this paper: human-LCAT

Title : Draft Genome Sequence of Helicobacter fennelliae Strain MRY12-0050, Isolated from a Bacteremia Patient - Rimbara_2013_Genome.Announc_1_e00512
Author(s) : Rimbara E , Matsui M , Mori S , Suzuki S , Suzuki M , Kim H , Sekizuka T , Kuroda M , Shibayama K
Ref : Genome Announc , 1 : , 2013
Abstract : Helicobacter fennelliae, a human enterohepatic pathogen, causes bacteremia and colitis. We isolated H. fennelliae strain MRY12-0050 from a female patient; this strain was isolated from 2 other patients from the same hospital during the same period, suggesting human-to-human transmission. This is the first report of an H. fennelliae genome sequence.
ESTHER : Rimbara_2013_Genome.Announc_1_e00512
PubMedSearch : Rimbara_2013_Genome.Announc_1_e00512
PubMedID: 23929465

Title : Distinguishable epidemics of multidrug-resistant Salmonella Typhimurium DT104 in different hosts - Mather_2013_Science_341_1514
Author(s) : Mather AE , Reid SW , Maskell DJ , Parkhill J , Fookes MC , Harris SR , Brown DJ , Coia JE , Mulvey MR , Gilmour MW , Petrovska L , de Pinna E , Kuroda M , Akiba M , Izumiya H , Connor TR , Suchard MA , Lemey P , Mellor DJ , Haydon DT , Thomson NR
Ref : Science , 341 :1514 , 2013
Abstract : The global epidemic of multidrug-resistant Salmonella Typhimurium DT104 provides an important example, both in terms of the agent and its resistance, of a widely disseminated zoonotic pathogen. Here, with an unprecedented national collection of isolates collected contemporaneously from humans and animals and including a sample of internationally derived isolates, we have used whole-genome sequencing to dissect the phylogenetic associations of the bacterium and its antimicrobial resistance genes through the course of an epidemic. Contrary to current tenets supporting a single homogeneous epidemic, we demonstrate that the bacterium and its resistance genes were largely maintained within animal and human populations separately and that there was limited transmission, in either direction. We also show considerable variation in the resistance profiles, in contrast to the largely stable bacterial core genome, which emphasizes the critical importance of integrated genotypic data sets in understanding the ecology of bacterial zoonoses and antimicrobial resistance.
ESTHER : Mather_2013_Science_341_1514
PubMedSearch : Mather_2013_Science_341_1514
PubMedID: 24030491

Title : Pepsinogen I\/II ratio is related to glucose, triacylglycerol, and uric acid levels - Tanaka_2012_Nutrition_28_418
Author(s) : Tanaka M , Fukui M , Kuroda M , Yamazaki M , Hasegawa G , Oda Y , Naito Y , Toda H , Yoshikawa T , Nakamura N
Ref : Nutrition , 28 :418 , 2012
Abstract : OBJECTIVE: Under- and overnutrition are associated with a worse prognosis and constitute independent risk factors for morbidity and mortality. It is increasingly important to understand the factors that affect nutritional and metabolic statuses. The purpose of this study was to assess the relation between the pepsinogen I/II ratio and several biochemical markers. METHODS: A cross-sectional study was performed in 1985 subjects who underwent a health screening test. Subjects had no medications for hyperuricemia, dyslipidemia, diabetes mellitus, or hypertension. All subjects were classified into two groups. Subjects with a pepsinogen I/II ratio below 3 were defined as having atrophic gastritis. The relations between the pepsinogen I/II ratio and several biochemical markers, including total cholesterol, triacylglycerol, uric acid, cholinesterase, and glucose levels, were evaluated. RESULTS: The presence of atrophic gastritis was significantly associated with age, smoking status, alcohol consumption, body mass index, and triacylglycerol, uric acid, cholinesterase, and hemoglobin levels. Multiple linear regression analysis demonstrated that the pepsinogen I/II ratio was an independent determinant of glucose level (beta = 0.104, P < 0.0001), triacylglycerol level (beta = 0.072, P = 0.0014), uric acid level (beta = 0.048, P = 0.0138), and hemoglobin (beta = 0.037, P = 0.0429) after adjustments for age, sex, smoking status, alcohol consumption, and body mass index. CONCLUSION: The pepsinogen I/II ratio was related to glucose, triacylglycerol, and uric acid levels. Such an association fosters the idea that a decreased pepsinogen I/II ratio seems favorable for the prevention of overnutrition.
ESTHER : Tanaka_2012_Nutrition_28_418
PubMedSearch : Tanaka_2012_Nutrition_28_418
PubMedID: 22304859

Title : Corynebacterium ulcerans 0102 carries the gene encoding diphtheria toxin on a prophage different from the C. diphtheriae NCTC 13129 prophage - Sekizuka_2012_BMC.Microbiol_12_72
Author(s) : Sekizuka T , Yamamoto A , Komiya T , Kenri T , Takeuchi F , Shibayama K , Takahashi M , Kuroda M , Iwaki M
Ref : BMC Microbiol , 12 :72 , 2012
Abstract : BACKGROUND: Corynebacterium ulcerans can cause a diphtheria-like illness, especially when the bacterium is lysogenized with a tox gene-carrying bacteriophage that produces diphtheria toxin. Acquisition of toxigenicity upon phage lysogenization is a common feature of C. ulcerans and C. diphtheriae. However, because of a lack of C. ulcerans genome information, a detailed comparison of prophages has not been possible between these two clinically important and closely related bacterial species.
RESULTS: We determined the whole genome sequence of the toxigenic C. ulcerans 0102 isolated in Japan. The genomic sequence showed a striking similarity with that of Corynebacterium pseudotuberculosis and, to a lesser extent, with that of C. diphtheriae. The 0102 genome contained three distinct prophages. One of these, PhiCULC0102-I, was a tox-positive prophage containing genes in the same structural order as for tox-positive C. diphtheriae prophages. However, the primary structures of the individual genes involved in the phage machinery showed little homology between the two counterparts. CONCLUSION: Taken together, these results suggest that the tox-positive prophage in this strain of C. ulcerans has a distinct origin from that of C. diphtheriae NCTC 13129.
ESTHER : Sekizuka_2012_BMC.Microbiol_12_72
PubMedSearch : Sekizuka_2012_BMC.Microbiol_12_72
PubMedID: 22583953
Gene_locus related to this paper: corub-g0cw29 , corub-g0cz26

Title : Whole-genome analysis of Salmonella enterica serovar Typhimurium T000240 reveals the acquisition of a genomic island involved in multidrug resistance via IS1 derivatives on the chromosome - Izumiya_2011_Antimicrob.Agents.Chemother_55_623
Author(s) : Izumiya H , Sekizuka T , Nakaya H , Taguchi M , Oguchi A , Ichikawa N , Nishiko R , Yamazaki S , Fujita N , Watanabe H , Ohnishi M , Kuroda M
Ref : Antimicrobial Agents & Chemotherapy , 55 :623 , 2011
Abstract : Salmonella enterica serovar Typhimurium is frequently associated with life-threatening systemic infections, and the recent global emergence of multidrug resistance in S. enterica isolates from agricultural and clinical settings has raised concerns. In this study, we determined the whole-genome sequence of fluoroquinolone-resistant S. enterica serovar Typhimurium T000240 strain (DT12) isolated from human gastroenteritis in 2000. Comparative genome analysis revealed that T000240 displays high sequence similarity to strain LT2, which was originally isolated in 1940, indicating that progeny of LT2 might be reemerging. T000240 possesses a unique 82-kb genomic island, designated as GI-DT12, which is composed of multidrug resistance determinants, including a Tn2670-like composite transposon (class 1 integron [intI1, bla(oxa-30), aadA1, qacEDelta1, and sul1], mercury resistance proteins, and chloramphenicol acetyltransferase), a Tn10-like tetracycline resistance protein (tetA), the aerobactin iron-acquisition siderophore system (lutA and lucABC), and an iron transporter (sitABCD). Since GI-DT12 is flanked by IS1 derivatives, IS1-mediated recombination likely played a role in the acquisition of this genomic island through horizontal gene transfer. The aminoglycoside-(3)-N-acetyltransferase (aac(3)) gene and a class 1 integron harboring the dfrA1 gene cassette responsible for gentamicin and trimethoprim resistance, respectively, were identified on plasmid pSTMDT12_L and appeared to have been acquired through homologous recombination with IS26. This study represents the first characterization of the unique genomic island GI-DT12 that appears to be associated with possible IS1-mediated recombination in S. enterica serovar Typhimurium. It is expected that future whole-genome studies will aid in the characterization of the horizontal gene transfer events for the emerging S. enterica serovar Typhimurium strains.
ESTHER : Izumiya_2011_Antimicrob.Agents.Chemother_55_623
PubMedSearch : Izumiya_2011_Antimicrob.Agents.Chemother_55_623
PubMedID: 21098248
Gene_locus related to this paper: salty-ycfp

Title : Whole genome sequence of Staphylococcus saprophyticus reveals the pathogenesis of uncomplicated urinary tract infection - Kuroda_2005_Proc.Natl.Acad.Sci.U.S.A_102_13272
Author(s) : Kuroda M , Yamashita A , Hirakawa H , Kumano M , Morikawa K , Higashide M , Maruyama A , Inose Y , Matoba K , Toh H , Kuhara S , Hattori M , Ohta T
Ref : Proc Natl Acad Sci U S A , 102 :13272 , 2005
Abstract : Staphylococcus saprophyticus is a uropathogenic Staphylococcus frequently isolated from young female outpatients presenting with uncomplicated urinary tract infections. We sequenced the whole genome of S. saprophyticus type strain ATCC 15305, which harbors a circular chromosome of 2,516,575 bp with 2,446 ORFs and two plasmids. Comparative genomic analyses with the strains of two other species, Staphylococcus aureus and Staphylococcus epidermidis, as well as experimental data, revealed the following characteristics of the S. saprophyticus genome. S. saprophyticus does not possess any virulence factors found in S. aureus, such as coagulase, enterotoxins, exoenzymes, and extracellular matrix-binding proteins, although it does have a remarkable paralog expansion of transport systems related to highly variable ion contents in the urinary environment. A further unique feature is that only a single ORF is predictable as a cell wall-anchored protein, and it shows positive hemagglutination and adherence to human bladder cell associated with initial colonization in the urinary tract. It also shows significantly high urease activity in S. saprophyticus. The uropathogenicity of S. saprophyticus can be attributed to its genome that is needed for its survival in the human urinary tract by means of novel cell wall-anchored adhesin and redundant uro-adaptive transport systems, together with urease.
ESTHER : Kuroda_2005_Proc.Natl.Acad.Sci.U.S.A_102_13272
PubMedSearch : Kuroda_2005_Proc.Natl.Acad.Sci.U.S.A_102_13272
PubMedID: 16135568
Gene_locus related to this paper: stas1-q4a0b8 , stas1-q4a0z3 , stas1-q4a018 , stas1-q4a076 , stas1-q4a169 , stas1-q49uw5 , stas1-q49vf8 , stas1-q49vg1 , stas1-q49vk0 , stas1-q49w07 , stas1-q49w20 , stas1-q49we3 , stas1-q49wg7 , stas1-q49ws3 , stas1-q49x95 , stas1-q49xp4 , stas1-q49yj4 , stas1-q49zd4 , stas1-q49zs7

Title : Whole-genome sequencing of staphylococcus haemolyticus uncovers the extreme plasticity of its genome and the evolution of human-colonizing staphylococcal species - Takeuchi_2005_J.Bacteriol_187_7292
Author(s) : Takeuchi F , Watanabe S , Baba T , Yuzawa H , Ito T , Morimoto Y , Kuroda M , Cui L , Takahashi M , Ankai A , Baba S , Fukui S , Lee JC , Hiramatsu K
Ref : Journal of Bacteriology , 187 :7292 , 2005
Abstract : Staphylococcus haemolyticus is an opportunistic bacterial pathogen that colonizes human skin and is remarkable for its highly antibiotic-resistant phenotype. We determined the complete genome sequence of S.haemolyticus to better understand its pathogenicity and evolutionary relatedness to the other staphylococcal species. A large proportion of the open reading frames in the genomes of S.haemolyticus, Staphylococcus aureus, and Staphylococcus epidermidis were conserved in their sequence and order on the chromosome. We identified a region of the bacterial chromosome just downstream of the origin of replication that showed little homology among the species but was conserved among strains within a species. This novel region, designated the "oriC environ," likely contributes to the evolution and differentiation of the staphylococcal species, since it was enriched for species-specific nonessential genes that contribute to the biological features of each staphylococcal species. A comparative analysis of the genomes of S.haemolyticus, S.aureus, and S.epidermidis elucidated differences in their biological and genetic characteristics and pathogenic potentials. We identified as many as 82 insertion sequences in the S.haemolyticus chromosome that probably mediated frequent genomic rearrangements, resulting in phenotypic diversification of the strain. Such rearrangements could have brought genomic plasticity to this species and contributed to its acquisition of antibiotic resistance.
ESTHER : Takeuchi_2005_J.Bacteriol_187_7292
PubMedSearch : Takeuchi_2005_J.Bacteriol_187_7292
PubMedID: 16237012
Gene_locus related to this paper: stahj-q4l3b3 , stahj-q4l4l0 , stahj-q4l7a8 , stahj-q4l7d5 , stahj-q4l8k8 , stahj-q4l8w4 , stahj-q4l8z5 , stahj-q4l9j6 , stahj-q4l432 , stahj-q4l435 , stahj-q4l478 , stahj-q4l521 , stahj-q4l548 , stahj-q4l609 , stahj-q4l866 , stahj-q4l910 , stahj-q4l940 , stahj-q4lak5

Title : Efficacy of long-term dietary restriction of total calories, fat, iron, and protein in patients with chronic hepatitis C virus - Iwasa_2004_Nutrition_20_368
Author(s) : Iwasa M , Iwata K , Kaito M , Ikoma J , Yamamoto M , Takeo M , Kuroda M , Fujita N , Kobayashi Y , Adachi Y
Ref : Nutrition , 20 :368 , 2004
Abstract : OBJECTIVES: A diet restrictive in total calories, fat, iron, and protein intake reduces serum alanine aminotransferase levels in patients with long-term hepatitis C virus infection. However, whether long-term dietary therapy causes adverse effects such as malnutrition and anemia due to a shortage of energy intake is not clear. We evaluated the balance of energy intake and changes in physical and hematologic indices of nutrition after a long-term dietary therapy.
METHODS: Twenty-two patients with long-term hepatitis C virus infection that did not respond to or who were able or unwilling to take interferon therapy were enrolled in this study. Our prescriptions included 7 mg/d or less of iron, 30 kcal. kg(-1). d(-1) of energy, 1.1 to 1.2 g. kg(-1). d(-1) of protein, and a fat energy fraction of 20%. Patients were followed for 24 mo.
RESULTS: Mean body fat percentage was 24.6% at entry and was significantly reduced after the diet prescription. Mean serum ferritin decreased significantly from 376 ng/mL at entry to 141 ng/mL after 24 mo. Mean serum alanine aminotransferase levels decreased significantly from 66 to 49 IU/L. Mean levels of hemoglobin, serum albumin, and cholinesterase did not change significantly during the follow-up period.
CONCLUSIONS: These results suggest that restriction of energy, fat, iron, and protein intakes is safely tolerated, so its long-term use should be recommended to patients with long-term infection with hepatitis C virus.
ESTHER : Iwasa_2004_Nutrition_20_368
PubMedSearch : Iwasa_2004_Nutrition_20_368
PubMedID: 15043853

Title : Genome and virulence determinants of high virulence community-acquired MRSA - Baba_2002_Lancet_359_1819
Author(s) : Baba T , Takeuchi F , Kuroda M , Yuzawa H , Aoki K , Oguchi A , Nagai Y , Iwama N , Asano K , Naimi T , Kuroda H , Cui L , Yamamoto K , Hiramatsu K
Ref : Lancet , 359 :1819 , 2002
Abstract : BACKGROUND: A new type of meticillin-resistant Staphylococcus aureus (MRSA), designated community-acquired MRSA, is becoming increasingly noticeable in the community, some strains of which cause fatal infections in otherwise healthy individuals. By contrast with hospital-acquired MRSA, community-acquired MRSA is more susceptible to non b-lactam antibiotics. We investigated the high virulence potential of certain strains of this bacterium.
METHODS: We ascertained the whole genome sequence of MW2, a strain of community-acquired MRSA, by shotgun cloning and sequencing. MW2 caused fatal septicaemia and septic arthritis in a 16-month-old girl in North Dakota, USA, in 1998. The genome of this strain was compared with those of hospital-acquired MRSA strains, including N315 and Mu50. FINDINGS: Meticillin resistance gene (mecA) in MW2 was carried by a novel allelic form (type IVa) of staphylococcal cassette chromosome mec (SCCmec), by contrast with type II in N315 and Mu50. Type IVa SCCmec did not carry any of the multiple antibiotic resistance genes reported in type II SCCmec. By contrast, 19 additional virulence genes were recorded in the MW2 genome. All but two of these virulence genes were noted in four of the seven genomic islands of MW2. INTERPRETATION: MW2 carried a range of virulence and resistance genes that was distinct from those displayed on the chromosomes of extant S aureus strains. Most genes were carried by specific allelic forms of genomic islands in the MW2 chromosome. The combination of allelic forms of genomic islands is the genetic basis that determines the pathogenicity of medically important phenotypes of S aureus, including those of community-acquired MRSA strains.
ESTHER : Baba_2002_Lancet_359_1819
PubMedSearch : Baba_2002_Lancet_359_1819
PubMedID: 12044378
Gene_locus related to this paper: staau-d2uin3 , staau-LIP , staau-lipas , staau-MW0741 , staau-MW2456 , staau-q6gfm6 , staau-SA0011 , staau-SA0569 , staau-SA0572 , staau-SA0897 , staau-SA1143 , staau-SA2240 , staau-SA2306 , staau-SA2367 , staau-SA2422 , staau-SAV0321 , staau-SAV0446 , staau-SAV0457 , staau-SAV0655 , staau-SAV1014 , staau-SAV1765 , staau-SAV1793 , staau-SAV2188 , staau-SAV2350

Title : Whole genome sequencing of meticillin-resistant Staphylococcus aureus - Kuroda_2001_Lancet_357_1225
Author(s) : Kuroda M , Ohta T , Uchiyama I , Baba T , Yuzawa H , Kobayashi I , Cui L , Oguchi A , Aoki K , Nagai Y , Lian J , Ito T , Kanamori M , Matsumaru H , Maruyama A , Murakami H , Hosoyama A , Mizutani-Ui Y , Takahashi NK , Sawano T , Inoue R , Kaito C , Sekimizu K , Hirakawa H , Kuhara S , Goto S , Yabuzaki J , Kanehisa M , Yamashita A , Oshima K , Furuya K , Yoshino C , Shiba T , Hattori M , Ogasawara N , Hayashi H , Hiramatsu K
Ref : Lancet , 357 :1225 , 2001
Abstract : BACKGROUND: Staphylococcus aureus is one of the major causes of community-acquired and hospital-acquired infections. It produces numerous toxins including superantigens that cause unique disease entities such as toxic-shock syndrome and staphylococcal scarlet fever, and has acquired resistance to practically all antibiotics. Whole genome analysis is a necessary step towards future development of countermeasures against this organism.
METHODS: Whole genome sequences of two related S aureus strains (N315 and Mu50) were determined by shot-gun random sequencing. N315 is a meticillin-resistant S aureus (MRSA) strain isolated in 1982, and Mu50 is an MRSA strain with vancomycin resistance isolated in 1997. The open reading frames were identified by use of GAMBLER and GLIMMER programs, and annotation of each was done with a BLAST homology search, motif analysis, and protein localisation prediction. FINDINGS: The Staphylococcus genome was composed of a complex mixture of genes, many of which seem to have been acquired by lateral gene transfer. Most of the antibiotic resistance genes were carried either by plasmids or by mobile genetic elements including a unique resistance island. Three classes of new pathogenicity islands were identified in the genome: a toxic-shock-syndrome toxin island family, exotoxin islands, and enterotoxin islands. In the latter two pathogenicity islands, clusters of exotoxin and enterotoxin genes were found closely linked with other gene clusters encoding putative pathogenic factors. The analysis also identified 70 candidates for new virulence factors. INTERPRETATION: The remarkable ability of S aureus to acquire useful genes from various organisms was revealed through the observation of genome complexity and evidence of lateral gene transfer. Repeated duplication of genes encoding superantigens explains why S aureus is capable of infecting humans of diverse genetic backgrounds, eliciting severe immune reactions. Investigation of many newly identified gene products, including the 70 putative virulence factors, will greatly improve our understanding of the biology of staphylococci and the processes of infectious diseases caused by S aureus.
ESTHER : Kuroda_2001_Lancet_357_1225
PubMedSearch : Kuroda_2001_Lancet_357_1225
PubMedID: 11418146
Gene_locus related to this paper: staau-LIP , staau-lipas , staau-MW0741 , staau-MW2456 , staau-q6gfm6 , staau-SA0011 , staau-SA0569 , staau-SA0572 , staau-SA0897 , staau-SA1143 , staau-SA2240 , staau-SA2306 , staau-SA2367 , staau-SA2422 , staau-SAV0321 , staau-SAV0446 , staau-SAV0457 , staau-SAV0655 , staau-SAV1014 , staau-SAV1765 , staau-SAV1793 , staau-SAV2188 , staau-SAV2350 , staau-SAV2484 , staau-SAV2594