Xanthomonas translucens commandeers the host rate-limiting step in ABA biosynthesis for disease susceptibility

Plants are vulnerable to disease through pathogen manipulation of phytohormone levels, which otherwise regulate development, abiotic, and biotic responses. Here, we show that the wheat pathogen Xanthomonas translucens pv. undulosa elevates expression of the host gene encoding 9-cis-epoxycarotenoid dioxygenase (TaNCED-5BS), which catalyzes the rate-limiting step in the biosynthesis of the phytohormone abscisic acid and a component of a major abiotic stress-response pathway, to promote disease susceptibility. Gene induction is mediated by a type III transcription activator-like effector. The induction of TaNCED-5BS results in elevated abscisic acid levels, reduced host transpiration and water loss, enhanced spread of bacteria in infected leaves, and decreased expression of the central defense gene TaNPR1. The results represent an appropriation of host physiology by a bacterial virulence effector.

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Synthesis of GDP-Mannose and Mannosylglycerate from Labeled Mannose by Genetically Engineered Escherichia coli without Loss of Specific Isotopic Enrichment

Applied and Environmental Microbiology ◽

10.1128/aem.69.1.233-240.2003 ◽

2003 ◽

Vol 69 (1) ◽

pp. 233-240 ◽

Cited By ~ 11

Author(s):

Maria-Manuel Sampaio ◽

Helena Santos ◽

Winfried Boos

Keyword(s):

Escherichia Coli ◽

Cold Water ◽

Genetically Engineered ◽

Isotopic Enrichment ◽

Rhodothermus Marinus ◽

Phosphotransferase System ◽

Gene Encoding ◽

Rate Limiting Step ◽

Limiting Step ◽

Rate Limiting

ABSTRACT We report the construction of an Escherichia coli mutant that harbors two compatible plasmids and that is able to synthesize labeled 2-O-α-d-mannosyl-d-glycerate from externally added labeled mannose without the loss of specific isotopic enrichment. The strain carries a deletion in the manA gene, encoding phosphomannose isomerase. This deletion prevents the formation of fructose-6-phosphate from mannose-6-phosphate after the uptake of mannose from the medium by mannose-specific enzyme II of the phosphotransferase system (PtsM). The strain also has a deletion of the cps gene cluster that prevents the synthesis of colanic acid, a mannose-containing polymer. Plasmid-encoded phosphomannomutase (cpsG) and mannose-1-phosphate guanylyltransferase (cpsB) ensure the formation of GDP-mannose. A second plasmid harbors msg, a gene from Rhodothermus marinus that encodes mannosylglycerate synthase, which catalyzes the formation of 2-O-α-d-mannosyl-d-glycerate from GDP-mannose and endogenous glycerate. The rate-limiting step in 2-O-α-d-mannosyl-d-glycerate formation is the transfer of GDP-mannose to glycerate. 2-O-α-d-mannosyl-d-glycerate can be released from cells by treatment with cold-water shock. The final product is formed in a yield exceeding 50% the initial quantity of labeled mannose, including loss during preparation and paper chromatography.

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Kaleidoscope

The British Journal of Psychiatry ◽

10.1192/bjp.205.4.334 ◽

2014 ◽

Vol 205 (4) ◽

pp. 334-335

Author(s):

Derek K. Tracy ◽

Dan W. Joyce ◽

Sukhwinder S. Shergill

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Genetic Variant ◽

Age At Onset ◽

Epidemiological Data ◽

Gene Encoding ◽

Rate Limiting Step ◽

Limiting Step ◽

The Impact ◽

Rate Limiting

It cannot have escaped our readers' notice that there has been a public increase in the awareness of the impact of dementia on people's lives: politicians have raised concerns about a dementia ‘time bomb’ as a greater number of people live to an older age; and even the 2013 G8 summit declared1 that there was a need for international initiatives to tackle this illness. The inevitable call for more research is underscored by the lack of any new licenced medications for Alzheimer's disease since 2002. There has been much interest in a putative role for statins – which inhibit the HMGCR enzyme, the rate-limiting step in cholesterol production – as retrospective epidemiological data have shown that they can reduce the risk of developing Alzheimer's disease by up to 70%; but, frustratingly, administration of these drugs to those with the illness appears to produce little benefit. Recent data have now shown that the gene encoding this HMGCR enzyme is a potent modifier for the age at onset and rate of conversion from mild cognitive impairment to Alzheimer's disease.2 Indeed, this work would indicate that its G-negative allele is second only to APOE2 as the most common and important protective genetic variant for spontaneous Alzheimer's disease.

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EDEM2 initiates mammalian glycoprotein ERAD by catalyzing the first mannose trimming step

The Journal of Cell Biology ◽

10.1083/jcb.201404075 ◽

2014 ◽

Vol 206 (3) ◽

pp. 347-356 ◽

Cited By ~ 81

Author(s):

Satoshi Ninagawa ◽

Tetsuya Okada ◽

Yoshiki Sumitomo ◽

Yukiko Kamiya ◽

Koichi Kato ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Enzymatic Activity ◽

Mammalian Cells ◽

Gene Knockout ◽

Human Cell Line ◽

Transcription Activator ◽

Rate Limiting Step ◽

Limiting Step ◽

Glycoprotein Degradation ◽

Rate Limiting

Glycoproteins misfolded in the endoplasmic reticulum (ER) are subjected to ER-associated glycoprotein degradation (gpERAD) in which Htm1-mediated mannose trimming from the oligosaccharide Man8GlcNAc2 to Man7GlcNAc2 is the rate-limiting step in yeast. In contrast, the roles of the three Htm1 homologues (EDEM1/2/3) in mammalian gpERAD have remained elusive, with a key controversy being whether EDEMs function as mannosidases or as lectins. We therefore conducted transcription activator-like effector nuclease–mediated gene knockout analysis in human cell line and found that all endogenous EDEMs possess mannosidase activity. Mannose trimming from Man8GlcNAc2 to Man7GlcNAc2 is performed mainly by EDEM3 and to a lesser extent by EDEM1. Most surprisingly, the upstream mannose trimming from Man9GlcNAc2 to Man8GlcNAc2 is conducted mainly by EDEM2, which was previously considered to lack enzymatic activity. Based on the presence of two rate-limiting steps in mammalian gpERAD, we propose that mammalian cells double check gpERAD substrates before destruction by evolving EDEM2, a novel-type Htm1 homologue that catalyzes the first mannose trimming step from Man9GlcNAc2.

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Solid products and rate-limiting step in the thermal half decomposition of natural dolomite in a CO2(g) atmosphere

Thermochimica Acta ◽

10.1016/s0040-6031(02)00603-2 ◽

2003 ◽

Cited By ~ 1

Author(s):

D Beruto

Keyword(s):

Rate Limiting Step ◽

Limiting Step ◽

Rate Limiting

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Ornithine Decarboxylase Activity in Cultured Endothelial Cells Stimulated by Serum, Thrombin and Serotonin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646709 ◽

1978 ◽

Vol 39 (02) ◽

pp. 496-503 ◽

Cited By ~ 8

Author(s):

P A D’Amore ◽

H B Hechtman ◽

D Shepro

Keyword(s):

Endothelial Cells ◽

Ornithine Decarboxylase ◽

Decarboxylase Activity ◽

Aortic Endothelial Cells ◽

Ornithine Decarboxylase Activity ◽

Rate Limiting Step ◽

Bovine Aortic Endothelial Cells ◽

Limiting Step ◽

Rate Limiting ◽

Serum Serotonin

SummaryOrnithine decarboxylase (ODC) activity, the rate-limiting step in the synthesis of polyamines, can be demonstrated in cultured, bovine, aortic endothelial cells (EC). Serum, serotonin and thrombin produce a rise in ODC activity. The serotonin-induced ODC activity is significantly blocked by imipramine (10-5 M) or Lilly 11 0140 (10-6M). Preincubation of EC with these blockers together almost completely depresses the 5-HT-stimulated ODC activity. These observations suggest a manner by which platelets may maintain EC structural and metabolic soundness.

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