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A Vivian

Publications and source records attributed to A Vivian.

At least 19 recordsLinked to original sources
PubMed2000

Cultivar-specific avirulence and virulence functions assigned to avrPphF in Pseudomonas syringae pv. phaseolicola, the cause of bean halo-blight disease.

The avrPphF gene was cloned from Pseudomonas syringae pathovar phaseolicola (PPH:) races 5 and 7, based on its ability to confer avirulence towards bean cultivars carrying the R1 gene for halo-blight resistance, such as Red Mexican. avrPphF comprised two open reading frames, which were both required for function, and was located on a 154 kb plasmid (pAV511) in PPH: Strain RW60 of PPH:, lacking pAV511, displayed a loss in virulence to a range of previously susceptible cultivars such as Tendergreen and Canadian Wonder. In Tendergreen virulence was restored to RW60 by avrPphF alone, whereas subcloned avrPphF in the absence of pAV511 greatly accelerated the hypersensitive resistance reaction caused by RW60 in Canadian Wonder. A second gene from pAV511, avrPphC, which controls avirulence to soybean, was found to block the activity of avrPphF in Canadian Wonder, but not in Red Mexican. avrPphF also conferred virulence in soybean. The multiple functions of avrPphF illustrate how effector proteins from plant pathogens have evolved to be recognized by R gene products and, therefore, be classified as encoded by avirulence genes.

Base Sequence↗
PubMed1999

Identification of a pathogenicity island, which contains genes for virulence and avirulence, on a large native plasmid in the bean pathogen Pseudomonas syringae pathovar phaseolicola.

The 154-kb plasmid was cured from race 7 strain 1449B of the phytopathogen Pseudomonas syringae pv. phaseolicola (Pph). Cured strains lost virulence toward bean, causing the hypersensitive reaction in previously susceptible cultivars. Restoration of virulence was achieved by complementation with cosmid clones spanning a 30-kb region of the plasmid that contained previously identified avirulence (avr) genes avrD, avrPphC, and avrPphF. Single transposon insertions at multiple sites (including one located in avrPphF) abolished restoration of virulence by genomic clones. Sequencing 11 kb of the complementing region identified three potential virulence (vir) genes that were predicted to encode hydrophilic proteins and shared the hrp-box promoter motif indicating regulation by HrpL. One gene achieved partial restoration of virulence when cloned on its own and therefore was designated virPphA as the first (A) gene from Pph to be identified for virulence function. In soybean, virPphA acted as an avr gene controlling expression of a rapid cultivar-specific hypersensitive reaction. Sequencing also revealed the presence of homologs of the insertion sequence IS100 from Yersinia and transposase Tn501 from P. aeruginosa. The proximity of several avr and vir genes together with mobile elements, as well as G+C content significantly lower than that expected for P. syringae, indicates that we have located a plasmid-borne pathogenicity island equivalent to those found in mammalian pathogens.

Bacterial Proteins↗
PubMed1999

Ocular abnormalities in Alagille syndrome.

OBJECTIVE: To assess the type and frequency of ocular abnormalities occurring in Alagille syndrome (AS) in a large group of affected patients and their parents and the potential pathogenetic role of fat-soluble vitamin deficiency. DESIGN: Observational case series. PARTICIPANTS: Twenty-two children with AS and 23 of their parents participated. MAIN OUTCOME MEASURES: Participants underwent full ophthalmic examination, including refraction, orthoptic examination, keratometry, slit-lamp examination, and funduscopy. Corneal diameter measurement was performed in a subset of nine and fluorescein angiography in a subset of six. Serum levels of vitamins A and E and cholesterol were measured. RESULTS: The most common ocular abnormalities in patients with AS were posterior embryotoxon (95%), iris abnormalities (45%), diffuse fundus hypopigmentation (57%, a previously unreported finding), speckling of the retinal pigment epithelium (33%), and optic disc anomalies (76%). Microcornea was not associated with large refractive errors, and visual acuity was not significantly affected by these ocular changes. Vitamin levels were normal. Ocular abnormalities including posterior embryotoxon, iris abnormalities, and optic disc or fundus pigmentary changes were detected in one parent in 36% of cases. CONCLUSIONS: Alagille syndrome is associated with a characteristic group of ocular findings without apparent serious functional significance and probably unrelated to fat-soluble vitamin deficiency. Simple ophthalmic examination of children with neonatal cholestatic jaundice and their parents should allow early diagnosis of AS, eliminating the need for extensive and invasive investigations.

Abnormalities, Drug-Induced↗
PubMed1999

A dispensable region of the chromosome which is associated with an avirulence gene in Pseudomonas syringae pv. pisi.

Pseudomonas syringae pv. pisi comprises a number of races which fall into two phylogenetically distinct groups (designated I and II). Races are based on cultivar specificity in the host plant, pea (Pisum sativum), and are specified by the presence of avirulence genes. The avirulence gene avrPpiA1 is present on the chromosome of all strains examined in race 2, which belongs to phylogenetic group II. A race 4B strain, from phylogenetic group I, lacks this avirulence gene and a comparative study was made of the chromosome in strains representing these two races. A race 2 cosmid clone (pAV270) carrying avrPpiA1 was used as a basis for collinearity analysis of races 2 and 4B. A region of the chromosome amounting to 8.5 kb and including avrPpiA1 was absent from race 4B compared with race 2. A fragment spanning the junction of the discontinuity in race 4B was isolated, cloned and used to delimit the extent of the additional DNA present in race 2. In both races the borders of the discontinuity contained DNA sequences which showed a high degree of conservation. A 7 bp slightly imperfect direct repeat (CCAGC(T)/(A)T) flanked the additional DNA in race 2, with a single copy in race 4B. The region flanking the additional DNA was present in all races of P. syringae pv. pisi. These results confirm the phylogenetic groupings in P. syringae pv. pisi.

Base Sequence↗
PubMed1998

A tellurite-resistance genetic determinant from phytopathogenic pseudomonads encodes a thiopurine methyltransferase: evidence of a widely-conserved family of methyltransferases.

A tellurite-resistance genetic determinant was isolated from the pea blight pathogen Pseudomonas syringae pathovar pisi by a shotgun strategy involving a tellurite-selective screening in Escherichia coli. A 1.65 kb tellurite resistance insert was obtained and analysed. It harbours a single complete and functional ORF encoding a deduced protein of 24, 445 Da. The deduced AA sequence shows significant similarities with the complete human thiopurine methyltransferase enzyme, a methyltransferase from Synechocystis and a methyltransferase-like sequence from Bordetella pertussis. The encoded thiopurine methyltransferase activity was demonstrated using a radiochemical microassay for the methylation of 6-mercaptopurine. This gene was detected in most P. syringae legume pathogens.

Amino Acid Sequence↗
PubMed1993

Changes in cultivar-specificity toward pea can result from transfer of plasmid RP4 and other incompatibility group P1 replicons to Pseudomonas syringae pv. pisi.

Transfer of RP4 and related replicons belonging to the Escherichia coli incompatibility group P (Pseudomonas aeruginosa IncP1) to races 2 and 6 of P. syringae pv. pisi was associated with the creation of two types of transconjugant, one resembling the parental race and the other showing an altered cultivar-specificity towards pea. The latter, irrespective of the parental race, exhibited a novel pattern of interaction with pea that corresponded to race 4; consequently such transconjugants were termed race 4-like. Curing of RP4 did not affect the phenotype, except in relation to the antibiotic resistances specified by RP4. The race 4-like strains were non-fluorescent when cultured on appropriate media (in contrast to the particular isolates of races 2 and 6 from which they were derived), showed an enhanced ability to inherit RP4 subsequently (at frequencies up to 10(-1) per recipient) and differed from their parental race in their pattern of plasmid profile. The plasmid profiles were similar for all race 4-like strains irrespective of origin. There was no evidence that RP4 had recombined with DNA in the recipient and probing failed to detect the retention of any part of RP4 in cured strains. The inheritance of the related cosmid vector, pLAFR3, had similar effects in races 2 and 6. This observation is important since this vector has been widely used to clone avirulence genes in plant pathogenic bacteria. Transfer of the IncW plasmids S-a and R388 did not cause any changes in the fluorescence or cultivar-specificity of races 2 or 6.(ABSTRACT TRUNCATED AT 250 WORDS)

Conjugation, Genetic↗
PubMed1992

Functional homologs of the Arabidopsis RPM1 disease resistance gene in bean and pea.

We showed that a bacterial avirulence (avr) gene function, avrPpiA1, from the pea pathogen Pseudomonas syringae pv pisi, is recognized by some, but not all, genotypes of Arabidopsis. Thus, an avr gene functionally defined on a crop species is also an avr gene on Arabidopsis. The activity of avrPpiA1 on a series of Arabidopsis genotypes is identical to that of the avrRpm1 gene from P.s. pv maculicola previously defined using Arabidopsis. The two avr genes are homologous and encode nearly identical predicted products. Moreover, this conserved avr function is also recognized by some bean and pea cultivars in what has been shown to be a gene-for-gene manner. We further demonstrated that the Arabidopsis disease resistance locus, RPM1, conditioning resistance to avrRpm1, also conditions resistance to bacterial strains carrying avrPpiA1. Therefore, bean, pea, and conceivably other crop species contain functional and potentially molecular homologs of RPM1.

Amino Acid Sequence↗
PubMed1991

Molecular genetics of Pseudomonas syringae pathovar pisi: plasmid involvement in cultivar-specific incompatibility.

A mutant (PF24) of the race 1 strain, 299A, of Pseudomonas syringae pv. pisi has been characterized in terms of its interactions with pea (Pisum sativum) cultivars. The mutant showed a changed reaction (avirulence to virulence) with a group of pea cultivars, including cvs. Belinda and Puget, previously thought to contain resistance genes R1 and R3. Avirulence towards cv. Puget was restored by transfer of any one of five cosmid clones from a race 3 (strain 870A) gene library to a rifampicin-resistant derivative of PF24. These observations were in agreement with a revised race-specific resistance genotype for Belinda and similar cultivars comprising a single resistance gene, R3. An incompatible interaction was observed between strain PF24 and cvs. Vinco (postulated to harbour race-specific resistance genes R1, R2, R3 and R5) and Hurst's Greenshaft (R4 and possibly R1), indicating that the mutant retains at least one avirulence gene (A1 or A1 and A4). Mutant PF24 showed loss of a cryptic plasmid (pAV212) compared with its progenitor, strain 299A. A subclone (pAV233) of one of the race 3 restoration clones showed strong hybridization with similar-sized digestion fragments in race 3 plasmid DNA, confirming the A3 gene to be plasmid-borne. Strong cross-hybridization was also observed with a single 3.27 kb EcoRI fragment of plasmid DNA present in strain 299A but absent from strain PF24. This is consistent with the corresponding A3 determinant being located on pAV212 in the race 1 strain 299A. The novel avirulence gene corresponding to A3 in strain 870A is provisionally designated avrPpi3.(ABSTRACT TRUNCATED AT 250 WORDS)

Blotting, Southern↗
PubMed1985

Molecular analysis of an antibiotic resistance plasmid, pAV5, and its derivative plasmids in Acinetobacter calcoaceticus.

The non-conjugative plasmid pAV5 specifies resistance to kanamycin/neomycin (KmR) and tetracycline (TcR). Physical evidence is presented to show that pAV5 gives rise to two plasmids, pAV51 (KmR) and pAV52 (TcR), which are formed by deletion of apparently non-overlapping segments of pAV5. Expression of TcR has been obtained in Escherichia coli and is associated with a 1.9 kb HindIII fragment found in pAV5 and in pAV52. Expression of KmR has been obtained in E. coli and is associated with a 1.3 kb PstI fragment found in pAV5 and pAV51. Evidence is presented that the KmR gene is flanked by inverted repeat sequences and is therefore tentatively identified as a transposon, designated Tn4411. The KmR gene specifies an aminoglycoside 3'-phosphotransferase-type I (APH(3')-I) enzyme.

Acinetobacter↗
PubMed1984

Isolation, characterization and mapping of mandelate pathway mutants of Acinetobacter calcoaceticus.

Mutants of Acinetobacter calcoaceticus EBF 65/65 that could not grow on intermediates of the mandelate or benzyl alcohol pathways were isolated and in some cases the enzymic lesions were identified. Several catabolic markers were mapped using the plasmid pAV1. The mandelate genes appeared to be clustered near the auxotrophic marker phe-1 but were not all contiguous with each other. The gene responsible for the appearance of the novel L(+)-mandelate dehydrogenase appeared to be close to a gene responsible for the activity of the original D(-)-mandelate dehydrogenase.

Acinetobacter↗
PubMed1980

Naturally occurring plasmids in Acinetobacter calcoaceticus: a P class R factor of restricted host range.

A naturally occurring transmissible plasmid, designated pAV1, has been isolated in Acinetobacter calcoaceticus. It specifies resistance to sulphonamides and is capable of mobilizing two non-transmissible resistance determinants for tetracycline and neomycin, respectively, within strains of A. calcoaceticus. It is incompatible with the P class R factors RP4 and R751 in A. calcoaceticus. On this basis we conclude that pAV1 is a member of the P incompatibility group. However, unlike most other P group R factors, pAV1 is not transmissible to strains of Escherichia coli, Pseudomonas aeruginosa, Klebsiella or Proteus mirabilis.

Acinetobacter↗
PubMed1980

Gene transfer in Acinetobacter calcoaceticus: fertility variants of the sex factor pAV1.

The naturally occurring transmissible plasmid pAV1 mediates chromosome transfer and can exhibit two distinct levels of transmissibility in Acinetobacter calcoaceticus strain EBF65/65. The two states of pAV1 have been arbitrarily designated pAV1a (low frequency variant) and pAV1b (high frequency variant). Both variants have the same incompatibility and host range properties and each mobilizes two non-transmissible resistance determinants for tetracycline and neomycin. Sex factor activity has been shown to be stable: however, pAV1b fertility variants can be derived from pAV1a donors following conjugal transfer of pAV1 into new recipient strains of EBF65/65.

Acinetobacter↗
PubMed1980

Naturally occurring plasmids in Acinetobacter calcoaceticus: pAV2, a plasmid which influences the fertility of the sex factor pAV1.

Acinetobacter calcoaceticus strain EBF65/65 harbours a cryptic plasmid, pAV2, which has been shown by electrophoretic separation on agarose gels to have a molecular mass of approximately 13.5 megadaltons (Md). Transfer of the previously described sex factor pAV1 (Hinchliffe & Vivian, 1980 a,b) from the hospital strainJC17 into strains possessing pAV2 occurs only at a low frequency, whereas transfer to similar strains lacking pAV2 occurs at a much higher frequency. In EBF65/65, pAV1 may be present in strains possessing or lacking pAV2; pAV1 strains lacking pAV2 correspond to strains previously described as pAV1a (Hinchliffe & Vivian, 1980b) whereas pAV1 strains which also possess pAV2 correspond to pAB1b strains. The genetic evidence presented here is consistent with the hypothesis that pAV2 specifies a host restriction and modification system that is active against pAV1. Physical evidence from agarose gel electrophoresis indicates that pAV1 corresponds to a band of approximately 85 Md in strain JC17. The corresponding band in strains of EBF65/65 is difficult to distinguish because of the presence of a further cryptic plasmid band of approximately 88 Md, designated pAV3. A small cryptic plasmid of approximately 6 Md, designated pAV4, is reported for EBF65/65.

Acinetobacter↗
PubMed1980

Restriction mediated by pAV2 affects the transfer of plasmids in Acinetobacter calcoaceticus.

The naturally occurring plasmid pAV2 restricts the entry of the P class plasmid RP4 and the W class plasmids R388 and S-a into Acinetobacter calcoaceticus strain EBF65/65 from Escherichia coli. The W class plasmids only transfer from E. coli into pAV2-strains. Plasmid RP4 is modified in the presence of pAV2 such that it is no longer restricted on entry into pAV2 recipients of strain EBF65/65.

Acinetobacter↗