Conditions for mutagenesis by N-methyl-N′-nitro-N-nitrosoguanidine and relationships of A. tumefaciens mutants to crown-gall tumor induction

Langley, Robert; Kado, Clarence I.

doi:10.1016/0027-5107(72)90014-0

Cited by 80 publications

(35 citation statements)

References 25 publications

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“…When we tested the tumour-inducing ability of the bald strain NT1REB on sunflower plants, a test host strain that is useful for virulence assessments based on tumour size and tumour fresh weight (Langley and Kado, 1972), and on red-potato tuber disks for quantitative estimates of virulence (Pueppke and Benny, 1981), we found that the size and weight of the tumours were consistently smaller than that induced by the wildtype C58 strain (Fig. 8).…”

Section: Effect Of Bald Strain On Virulencementioning

confidence: 99%

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**Characterization of flagella genes of Agrobacterium tumefaciens, and the effect of a bald strain on virulence**

Chesnokova

Coutinho

Khan

et al. 1997

Molecular Microbiology

104

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Because the 54 promoter is associated with genes regulated by physiological changes in various bacteria, the flaC gene might be similarly regulated in response to A. tumefaciens responding to host plant stimuli. Virulence studies showed that the bald strain was consistently reduced in virulence below that of the parental wild-type strain by at least 38%. The difference is statistically significant and suggests that the flagella may play a role in facilitating virulence.

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Section: Effect Of Bald Strain On Virulencementioning

confidence: 99%

“…Russian Mammouth) and on Jimson weed (D. stramonium) as described previously (Langley and Kado, 1972). The stems of five-week-old seedlings of these plants were inoculated with 10 7 cells ml ¹1 of test and control inocula, and four-week-old crown-gall tumours appearing at the inoculation site were cut away from the stem with a scapel.…”

Section: Virulence Assaymentioning

confidence: 99%

**Characterization of flagella genes of Agrobacterium tumefaciens, and the effect of a bald strain on virulence**

Chesnokova

Coutinho

Khan

et al. 1997

Molecular Microbiology

104

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“…X. oryzae pv. oryzae strains belonging to races 0 to 6 were grown in either medium PSA (35) or medium 925 (20) supplemented with 0.1% yeast extract. The antibiotics incorporated in the media when appropriate were kanamycin (20 pg/ml) and ampicillin (100 pg/ml).…”

mentioning

confidence: 99%

Restoration of pathogenicity of avirulent Xanthomonas oryzae pv. oryzae and X. campestris pathovars by reciprocal complementation with the hrpXo and hrpXc genes and identification of HrpX function by sequence analyses

1993

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The molecular basis of pathogenesis by Xanthomonas oryzae pv. oryzae has been partly elucidated by the identification of a gene, hrpXo, required for bacterial blight on rice. A mutation in hrpXo results in the loss of pathogenicity on rice and the loss of hypersensitivity on nonhosts such as Datura stramonium and radishes. Pathogenicity and its ability to cause Xanthomonas oryzae pv. oryzae (30), a yellow-pigmented gram-negative member of the family Pseudomonadaceae, causes bacterial blight on rice, a disease of considerable importance in the lowland rice-growing regions of the world (21). X. oryzae pv. oryzae infects through natural openings by first multiplying at that site and then invading primarily the vascular tissues by propagating in the xylem (22, 31). Severe necrosis along the interveinal regions, known as leaf blight, occurs as a result of pathogen ingression and multiplication.X. campestris pv. campestris causes the black rot disease of cruciferous plants. Like X. oryzae pv. oryzae, X. campestnis pv. campestris enters through natural openings, mainly hydathodes located along the leaf edge. This organism propagates in the xylem, which results in the necrosis of interveinal tissues and blackening along the veins.For both bacteria, the mechanism of pathogenesis is poorly understood. this gene, designated hrpXo (for hypersensitive reaction pathogenicity), has been examined by protein sequence analysis. Unlike the so-called avirulence (avr) genes, whose products catalyze the formation of metabolites that differentially elicit hypersensitivity responses on incompatible cultivars of a particular host (recently reviewed in references 14, 17a, 27, and 38), the hrpX gene product prevents a vascular hypersensitivity response (VHR), which is a rapid tissue necrosis in the vascular system, in the respective compatible host (17).The clustered hrp genes that are likely involved in secretion (7) and that are unrelated to hrpX have been studied with X. campestris pv. campestris (1)

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“…Escherichia coli strains were cultured in Luria-Bertani medium (32) at 370C. A. tumefaciens strains were grown in 523 medium (20) and minimal 925 medium (25) at 290C. Antibiotics were added at the following concentrations (in micrograms per milliliter) shown in parentheses: ampicillin (50), chloramphenicol (20), gentamicin (3), kanamycin (15), neomycin (30), tetracycline (10), and spectinomycin (50) for E. coli; and chloramphenicol (3), gentamicin (15), kanamycin (20), neomy-5698 CHEN AND KADO (21) and cleaved with appropriate restriction endonucleases, and the resulting DNA fragments were separated by agarose gel electrophoresis for molecular cloning (38).…”

Section: Methodsmentioning

confidence: 99%

“…Plasmids with deletions and TnCAT insertions were introduced into A. tumefaciens LBA4301 (pTiC58Trac) by electroporation. The resulting transformants were verified for the presence of the Ti plasmid by plasmid miniscreening (21) and growth on basal minimum 925 medium (25) containing 50 pug of nopaline per ml. Virulence was assayed by inoculating plant stems with A. tumefaciens strains that were grown for 2 days at 290C on 523 medium agar (1.5%) containing the appropriate antibiotics.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Agrobacterium tumefaciens oncogenicity by the osa gene of pSa

Chen

Kado

1994

J Bacteriol

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The IncW plasmid pSa originally derived from Shigella flexneri completely inhibits the tumor-inducing ability of Agrobacterium tumefaciens when it is resident in this organism. Oncogenic inhibition is mediated through the expression of the osa gene on pSa. This gene is part of a 3.1-kb DNA segment of pSa that contains four open reading frames revealed by sequencing. Specific deletions and TnCAT insertions within this segment localized the oncogenic inhibitory activity to the last open reading frame, orf-4, designated osa (for oncogenic suppression activity). No promoter exists immediately upstream of the coding sequence of osa since TnCAT insertions or deletions into orf-3 caused the loss of oncogenic inhibition. Deletion analysis showed that the promoter of orf-1 is required for osa transcription. The first three orfs have no role in oncogenic inhibition, since osa alone placed under the control of a constitutive Pkm promoter completely inhibited A. tumefaciens oncogenicity. This inhibition of oncogenicity by osa is not limited to a specific host plant but appears to show broad host specificity. Because the osa-encoded product has close homologies to the fiwA-encoded product of the IncP plasmid RP1, osa may be involved in fertility inhibition that would prevent or reduce the formation of stable mating pairs and T-DNA transfer between A. tumefaciens and plants.

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Conditions for mutagenesis by N-methyl-N′-nitro-N-nitrosoguanidine and relationships of A. tumefaciens mutants to crown-gall tumor induction

Cited by 80 publications

References 25 publications

**Characterization of flagella genes of Agrobacterium tumefaciens, and the effect of a bald strain on virulence**

**Characterization of flagella genes of Agrobacterium tumefaciens, and the effect of a bald strain on virulence**

Restoration of pathogenicity of avirulent Xanthomonas oryzae pv. oryzae and X. campestris pathovars by reciprocal complementation with the hrpXo and hrpXc genes and identification of HrpX function by sequence analyses

Inhibition of Agrobacterium tumefaciens oncogenicity by the osa gene of pSa

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