Journal articles: 'Gene nod'

1

Zuanazzi, José Angelo Silveira, Pierre Henri Clergeot, Jean-Charles Quirion, Henri-Philippe Husson, Adam Kondorosi, and Pascal Ratet. "Production of Sinorhizobium meliloti nod Gene Activator and Repressor Flavonoids from Medicago sativa Roots." Molecular Plant-Microbe Interactions® 11, no. 8 (August 1998): 784–94. http://dx.doi.org/10.1094/mpmi.1998.11.8.784.

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During symbiosis between leguminous plants and rhizobia, flavonoids exuded by the plants act as chemoattractants and nodulation (nod) gene regulators in the other partner. To better understand the role of these compounds during the early steps of the alfalfa-Sinorhizobium meliloti symbiosis and the regulation of their production we have isolated nod gene inducers from alfalfa roots. All the compounds that we identified in this study as nod gene inducers in the root are flavonoids, indicating that other compounds with nod gene activator capacity may have little contribution, if any, to nod gene activation. Most of the intermediates of the flavonoid pathway were found in Medicago sativa roots and nodules, but only end products of the flavonoid pathway were identified in the root exudate. We have also studied flavonoid production in different parts of the root and found that it is developmentally regulated during root growth. Finally, we have shown that coumestrol and medicarpin, present in the exudates and previously described as phytoalexins, possess nod gene repressing activity, indicating that the in vivo nod gene inducing activity of the root exudate results from positive as well as negative controls of nod gene expression by the flavonoids.

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Southwick, Audrey M., Lai-Xi Wang, Sharon R. Long, and Yuan C. Lee. "Activity of Sinorhizobium meliloti NodAB and NodH Enzymes on Thiochitooligosaccharides." Journal of Bacteriology 184, no. 14 (July 15, 2002): 4039–43. http://dx.doi.org/10.1128/jb.184.14.4039-4043.2002.

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ABSTRACT Rhizobium bacteria synthesize signal molecules called Nod factors that elicit responses in the legume root during nodulation. Nod factors, modified N-acylated β-(1,4)-N-acetylglucosamine, are synthesized by the nodulation (nod) gene products. We tested the ability of three Sinorhizobium meliloti nod gene products to modify Nod factor analogs with thio linkages instead of O-glycosidic bonds in the oligosaccharide backbone.

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Peck, Melicent C., Robert F. Fisher, and Sharon R. Long. "Diverse Flavonoids Stimulate NodD1 Binding to nod Gene Promoters in Sinorhizobium meliloti." Journal of Bacteriology 188, no. 15 (August 1, 2006): 5417–27. http://dx.doi.org/10.1128/jb.00376-06.

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ABSTRACT NodD1 is a member of the NodD family of LysR-type transcriptional regulators that mediates the expression of nodulation (nod) genes in the soil bacterium Sinorhizobium meliloti. Each species of rhizobia establishes a symbiosis with a limited set of leguminous plants. This host specificity results in part from a NodD-dependent upregulation of nod genes in response to a cocktail of flavonoids in the host plant's root exudates. To demonstrate that NodD is a key determinant of host specificity, we expressed nodD genes from different species of rhizobia in a strain of S. meliloti lacking endogenous NodD activity. We observed that nod gene expression was initiated in response to distinct sets of flavonoid inducers depending on the source of NodD. To better understand the effects of flavonoids on NodD, we assayed the DNA binding activity of S. meliloti NodD1 treated with the flavonoid inducer luteolin. In the presence of luteolin, NodD1 exhibited increased binding to nod gene promoters compared to binding in the absence of luteolin. Surprisingly, although they do not stimulate nod gene expression in S. meliloti, the flavonoids naringenin, eriodictyol, and daidzein also stimulated an increase in the DNA binding affinity of NodD1 to nod gene promoters. In vivo competition assays demonstrate that noninducing flavonoids act as competitive inhibitors of luteolin, suggesting that both inducing and noninducing flavonoids are able to directly bind to NodD1 and mediate conformational changes at nod gene promoters but that only luteolin is capable of promoting the downstream changes necessary for nod gene induction.

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Renier, Adeline, Fabienne Maillet, Joel Fardoux, Véréna Poinsot, Eric Giraud, and Nico Nouwen. "Photosynthetic Bradyrhizobium Sp. Strain ORS285 Synthesizes 2-O-Methylfucosylated Lipochitooligosaccharides for nod Gene–Dependent Interaction with Aeschynomene Plants." Molecular Plant-Microbe Interactions® 24, no. 12 (December 2011): 1440–47. http://dx.doi.org/10.1094/mpmi-05-11-0104.

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Bradyrhizobium sp. strain ORS285 is a photosynthetic bacterium that forms nitrogen-fixing nodules on the roots and stems of tropical aquatic legumes of the Aeschynomene genus. The symbiotic interaction of Bradyrhizobium sp. strain ORS285 with certain Aeschynomene spp. depends on the presence of nodulation (nod) genes whereas the interaction with other species is nod gene independent. To study the nod gene-dependent molecular dialogue between Bradyrhizobium sp. strain ORS285 and Aeschynomene spp., we used a nodB-lacZ reporter strain to monitor the nod gene expression with various flavonoids. The flavanones liquiritigenin and naringenin were found to be the strongest inducers of nod gene expression. Chemical analysis of the culture supernatant of cells grown in the presence of naringenin showed that the major Nod factor produced by Bradyrhizobium sp. strain ORS285 is a modified chitin pentasaccharide molecule with a terminal N-C18:1-glucosamine and with a 2-O-methyl fucose linked to C-6 of the reducing glucosamine. In this respect, the Bradyrhizobium sp. strain ORS285 Nod factor is the same as the major Nod factor produced by the nonphotosynthetic Bradyrhizobium japonicum USDA110 that nodulates the roots of soybean. This suggests a classic nod gene-dependent molecular dialogue between Bradyrhizobium sp. strain ORS285 and certain Aeschynomene spp. This is supported by the fact that B. japonicum USDA110 is able to form N2-fixing nodules on both the roots and stems of Aeschynomene afraspera.

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5

O'Neill, Luke. "Crohn's disease gene is given the NOD." Trends in Immunology 22, no. 8 (August 2001): 418–19. http://dx.doi.org/10.1016/s1471-4906(01)02002-6.

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6

Hogg, Bridget, Andrea E. Davies, Karen E. Wilson, Ton Bisseling, and J. Allan Downie. "Competitive Nodulation Blocking of cv. Afghanistan Pea Is Related to High Levels of Nodulation Factors Made by Some Strains of Rhizobium leguminosarum bv. viciae." Molecular Plant-Microbe Interactions® 15, no. 1 (January 2002): 60–68. http://dx.doi.org/10.1094/mpmi.2002.15.1.60.

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Cultivar Afghanistan peas are resistant to nodulation by many strains of Rhizobium leguminosarum bv. viciae but are nodulated by strain TOM, which carries the host specificity gene nodX. Some strains that lack nodX can inhibit nodulation of cv. Afghanistan by strain TOM. We present evidence that this “competitive nodulation-blocking” (Cnb) phenotype may result from high levels of Nod factors inhibiting nodulation of cv. Afghanistan peas. The TOM nod gene region (including nodX) is cloned on pIJ1095, and strains (including TOM itself) carrying pIJ1095 nodulate cv. Afghanistan peas very poorly but can nodulate other varieties normally. The presence of pIJ1095, which causes increased levels of Nod factor production, correlates with Cnb. Nodulation of cv. Afghanistan by TOM is also inhibited by a cloned nodD gene that increases nod gene expression and Nod factor production. Nodulation of cv. Afghanistan can be stimulated if nodD on pIJ1095 is mutated, thus severely reducing the level of Nod factor produced. Repression of nod gene expression by nolR eliminates the Cnb phenotype and can stimulate nodulation of cv. Afghanistan. Addition of Nod factors to cv. Afghanistan roots strongly inhibits nodulation. The Cnb+ strains and added Nod factors inhibit infection thread initiation by strain TOM. The sym2A allele determines resistance of cv. Afghanistan to nodulation by strains of R. leguminosarum bv. viciae lacking nodX. We tested whether sym2A is involved in Cnb by using a pea line carrying the sym2A region introgressed from cv. Afghanistan; nodulation in the introgressed line was inhibited by Cnb+ strains. Therefore, the sym2A region has an effect on Cnb, although another locus (or loci) may contribute to the stronger Cnb seen in cv. Afghanistan.

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Arai, Satoko, Christina Minjares, Seiho Nagafuchi, and Toru Miyazaki. "Improved Experimental Procedures for Achieving Efficient Germ Line Transmission of Nonobese Diabetic (NOD)-Derived Embryonic Stem Cells." Experimental Diabesity Research 5, no. 3 (2004): 219–26. http://dx.doi.org/10.1080/15438600490486877.

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The manipulation of a specific gene in NOD mice, the best animal model for insulin-dependent diabetes mellitus (IDDM), must allow for the precise characterization of the functional involvement of its encoded molecule in the pathogenesis of the disease. Although this has been attempted by the cross-breeding of NOD mice with many gene knockout mice originally created on the 129 or C57BL/6 strain background, the interpretation of the resulting phenotype(s) has often been confusing due to the possibility of a known or unknown disease susceptibility locus (e.g.,Iddlocus) cosegregating with the targeted gene from the diabetes-resistant strain. Therefore, it is important to generate mutant mice on a pure NOD background by using NOD-derived embryonic stem (ES) cells. By using the NOD ES cell line established by Nagafuchi and colleagues in 1999 (FEBSLett., 455, 101–104), the authors reexamined various conditions in the context of cell culture, DNA transfection, and blastocyst injection, and achieved a markedly improved transmission efficiency of these NOD ES cells into the mouse germ line. These modifications will enable gene targeting on a “pure” NOD background with high efficiency, and contribute to clarifying the physiological roles of a variety of genes in the disease course of IDDM.

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Dugas, V., A. Liston, E. E. Hillhouse, R. Collin, G. Chabot-Roy, A.-N. Pelletier, C. Beauchamp, K. Hardy, and S. Lesage. "Idd13 is involved in determining immunoregulatory DN T-cell number in NOD mice." Genes & Immunity 15, no. 2 (January 16, 2014): 82–87. http://dx.doi.org/10.1038/gene.2013.65.

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9

&NA;. "GAD65 gene therapy exhibits promise in NOD mice." Inpharma Weekly &NA;, no. 1345 (July 2002): 8. http://dx.doi.org/10.2165/00128413-200213450-00015.

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10

Banfalvi, Zsofia, Anthony Nieuwkoop, Maria Schell, Linda Besl, and Gary Stacey. "Regulation of nod gene expression in Bradyrhizobium japonicum." Molecular and General Genetics MGG 214, no. 3 (November 1988): 420–24. http://dx.doi.org/10.1007/bf00330475.

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11

Swanson, J. A., J. T. Mulligan, and S. R. Long. "Regulation of syrM and nodD3 in Rhizobium meliloti." Genetics 134, no. 2 (June 1, 1993): 435–44. http://dx.doi.org/10.1093/genetics/134.2.435.

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Abstract The early steps of symbiotic nodule formation by Rhizobium on plants require coordinate expression of several nod gene operons, which is accomplished by the activating protein NodD. Three different NodD proteins are encoded by Sym plasmid genes in Rhizobium meliloti, the alfalfa symbiont. NodD1 and NodD2 activate nod operons when Rhizobium is exposed to host plant inducers. The third, NodD3, is an inducer-independent activator of nod operons. We previously observed that nodD3 carried on a multicopy plasmid required another closely linked gene, syrM, for constitutive nod operon expression. Here, we show that syrM activates expression of the nodD3 gene, and that nodD3 activates expression of syrM. The two genes constitute a self-amplifying positive regulatory circuit in both cultured Rhizobium and cells within the symbiotic nodule. We find little effect of plant inducers on the circuit or on expression of nodD3 carried on pSyma. This regulatory circuit may be important for regulation of nod genes within the developing nodule.

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12

Heidstra, Renze, Gerd Nilsen, Francisco Martinez-Abarca, Ab van Kammen, and Ton Bisseling. "Nod Factor-Induced Expression of Leghemoglobin to Study the Mechanism of NH4NO3 Inhibition on Root Hair Deformation." Molecular Plant-Microbe Interactions® 10, no. 2 (March 1997): 215–20. http://dx.doi.org/10.1094/mpmi.1997.10.2.215.

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Nod factors secreted by Rhizobium leguminosarum bv. viciae induce root hair deformation, the formation of nodule primordia, and the expression of early nodulin genes in Vicia sativa (vetch). Root hair deformation is induced within 3 h in a small, susceptible zone (±2 mm) of the root. NH4NO3, known to be a potent blocker of nodule formation, inhibits root hair deformation, initial cortical cell divisions, and infection thread formation. To test whether NH4NO3 affects the formation of a component of the Nod factor perception-transduction system, we studied Nod factor-induced gene expression. The differential display technique was used to search for marker genes, which are induced within 1 to 3 h after Nod factor application. Surprisingly, one of the isolated cDNA clones was identified as a leghemoglobin gene (VsLb1), which is induced in vetch roots within 1 h after Nod factor application. By using the drug brefeldin A, it was then shown that VsLb1 activation does not require root hair deformation. The pVsLb1 clone was used as a marker to show that in vetch plants grown in the presence of NH4NO3 Nod factor perception and transduction leading to gene expression are unaffected.

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13

Guasch-Vidal, B., J. Estévez, M. S. Dardanelli, M. E. Soria-Díaz, F. Fernández de Córdoba, C. I. A. Balog, H. Manyani, et al. "High NaCl Concentrations Induce the nod Genes of Rhizobium tropici CIAT899 in the Absence of Flavonoid Inducers." Molecular Plant-Microbe Interactions® 26, no. 4 (April 2013): 451–60. http://dx.doi.org/10.1094/mpmi-09-12-0213-r.

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The nodulation (nod) genes of Rhizobium tropici CIAT899 can be induced by very low concentrations (micromolar to nanomolar range) of several flavonoid molecules secreted by the roots of leguminous plants under a number of different conditions. Some of these conditions have been investigated and appear to have a great influence on the concentration and the number of different Nod factors, which can induce root nodule primordia and pseudonodules in several leguminous plant roots. In one such condition, we added up to 300 mM NaCl to the induction medium of R. tropici CIAT899 containing the nod gene inducer apigenin. At the higher concentrations of NaCl, larger amounts and more different Nod factors were produced than in the absence of extra NaCl. To our surprise, under control conditions (300 mM NaCl without apigenin), some Nod-factor-like spots were also observed on the thin-layer plates used to detect incorporation of radiolabeled glucosamine into newly synthesized Nod factors. This phenomenon was further investigated with thin-layer plates, fusions of nod genes to the lacZ gene, high-performance liquid chromatography, mass spectrometry, and the formation of pseudonodules on bean roots. Here, we report that, in the absence of flavonoid inducers, high concentrations of NaCl induced nod genes and the production of Nod factors.

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14

Dugas, V., A. Liston, E. E. Hillhouse, R. Collin, G. Chabot-Roy, A.-N. Pelletier, C. Beauchamp, K. Hardy, and S. Lesage. "Erratum: Idd13 is involved in determining immunoregulatory DN T-cell number in NOD mice." Genes & Immunity 15, no. 4 (June 2014): 263. http://dx.doi.org/10.1038/gene.2014.15.

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15

Vernoud, Vanessa, Etienne-Pascal Journet, and David G. Barker. "MtENOD20, a Nod Factor-Inducible Molecular Marker for Root Cortical Cell Activation." Molecular Plant-Microbe Interactions® 12, no. 7 (July 1999): 604–14. http://dx.doi.org/10.1094/mpmi.1999.12.7.604.

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The spatio-temporal expression pattern of the Medicago truncatula ENOD20 gene during early stages of nodulation has been analyzed with transgenic alfalfa (M. varia) expressing a pMtENOD20-GUS chimeric fusion. Our results show that transcriptional activation of this gene occurs initially in dividing inner cortical cells corresponding to sites of nodule primordium formation and subsequently in root hairs containing infection threads. Use of Sinorhizobium meliloti nod gene mutants that uncouple nodule organogenesis from infection has confirmed that early MtENOD20 transcription is tightly linked to cortical cell activation (CCA). Furthermore, these experiments have revealed that an S. meliloti nodH mutant, defective in Nod factor sulfation and epidermal cell activation, is nevertheless able to elicit low-level CCA. Purified S. meliloti Nod factors trigger MtENOD20 transcription very rapidly (within 12 to 24 h) in the root cortex, and studies with transgenic alfalfa show that Nod factors are able to elicit gene expression coupled to CCA at concentrations as low as 10-11 M. Finally, we have made use of a range of synthetic lipo-chitooligosaccharides to show that fatty acid chain length is an important structural parameter in the capacity of Nod factors to elicit CCA. Taken together, our results suggest that pMtENOD20-GUS transgenic lines should prove valuable tools in future studies of Rhizobium and Nod factor-elicited CCA.

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Krause, Andrea, Vo T. T. Lan, and William J. Broughton. "Induction of Chalcone Synthase Expression by Rhizobia and Nod factors in Root Hairs and Roots." Molecular Plant-Microbe Interactions® 10, no. 3 (April 1997): 388–93. http://dx.doi.org/10.1094/mpmi.1997.10.3.388.

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Chalcone synthase (CHS) of Vigna unguiculata is encoded by a gene family that is abundantly transcribed in leaves and nodules. Inoculation with Rhizobium sp. NGR234, which nodulates V. unguiculata, or with NGRΔnodABC, a mutant deficient in Nod factor production, induced rapid accumulation of CHS mRNAs in roots and root hairs. As both Nod+ and Nod- bacteria provoke responses, induction of CHS gene expression may involve symbiotic or defense responses. Four days after inoculation with the wild-type Rhizobium sp., the transcript levels increased in roots but decreased in root hairs. Use of a region unique to the 5′ end of a specific CHS gene (VuCHS1) showed that increases of transcript levels in root hairs 24 h after inoculation with both rhizobia were specific to this gene. Transcripts of this gene in roots were only detectable 4 days after treatment with NGR234. It is possible therefore that accumulation of VuCHS1 follows the infection pathway of rhizobia entering legume roots. Purified Nod factors induced accumulation of transcripts, showing that they might be part of the signal transduction pathway leading to CHS expression.

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Swanson, Jean A., Janice K. Tu, Joy Ogawa, Raghu Sanga, Robert F. Fisher, and Sharon R. Long. "Extended Region of Nodulation Genes in Rhizobium meliloti 1021. I. Phenotypes of Tn5 Insertion Mutants." Genetics 117, no. 2 (October 1, 1987): 181–89. http://dx.doi.org/10.1093/genetics/117.2.181.

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ABSTRACT Rhizobium meliloti Nod- mutant WL131, a derivative of wild-type strain 102F51, was complemented by a clone bank of wild-type R. meliloti 1021 DNA, and clone pRmJT5 was recovered. Transfer of pRmJT5 conferred alfalfa nodulation on other Rhizobium species, indicating a role in host range determination for pRmJT5. Mutagenesis of pRmJT5 revealed several segments in which transposon insertion causes delay in nodulation, and/or marked reduction of the number of nodules formed on host alfalfa plants. The set of mutants indicated five regions in which nod genes are located; one mutant, nod-216, is located in a region not previously reported to encode a nodulation gene. Other mutant phenotypes correlated with the positions of open reading frames for nodH, nodF and nodE, and with a 2.2-kb Eco RI fragment. A mutant in nodG had no altered phenotype in this strain. One nodulation mutant was shown to be a large deletion of the common nod gene region. We present a discussion comparing the various studies made on this extended nod gene region.

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Rodpothong, Patsarin, John T. Sullivan, Kriangsak Songsrirote, David Sumpton, Kenneth W. J. T. Cheung, Jane Thomas-Oates, Simona Radutoiu, Jens Stougaard, and Clive W. Ronson. "Nodulation Gene Mutants of Mesorhizobium loti R7A—nodZ and nolL Mutants Have Host-Specific Phenotypes on Lotus spp." Molecular Plant-Microbe Interactions® 22, no. 12 (December 2009): 1546–54. http://dx.doi.org/10.1094/mpmi-22-12-1546.

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Rhizobial Nod factors induce plant responses and facilitate bacterial infection, leading to the development of nitrogen-fixing root nodules on host legumes. Nodule initiation is highly dependent on Nod-factor structure and, hence, on at least some of the nodulation genes that encode Nod-factor production. Here, we report the effects of mutations in Mesorhizobium loti R7A nodulation genes on nodulation of four Lotus spp. and on Nod-factor structure. Most mutants, including a ΔnodSΔnolO double mutant that produced Nod factors lacking the carbamoyl and possibly N-methyl groups on the nonreducing terminal residue, were unaffected for nodulation. R7AΔnodZ and R7AΔnolL mutants that produced Nod factors without the (acetyl)fucose on the reducing terminal residue had a host-specific phenotype, forming mainly uninfected nodule primordia on Lotus filicaulis and L. corniculatus and effective nodules with a delay on L. japonicus. The mutants also showed significantly reduced infection thread formation and Nin gene induction. In planta complementation experiments further suggested that the acetylfucose was important for balanced signaling in response to Nod factor by the L. japonicus NFR1/NFR5 receptors. Overall the results reveal differences in the sensitivity of plant perception with respect to signaling leading to root hair deformation and nodule primordium development versus infection thread formation and rhizobial entry.

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Richardson, AE, MA Djordjevic, BG Rolfe, and RJ Simpson. "Expression of Nodulation Genes in Rhizobium and Acid-Sensitivity of Nodule Formation." Functional Plant Biology 16, no. 1 (1989): 117. http://dx.doi.org/10.1071/pp9890117.

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The formation of nitrogen-fixing nodules on roots of leguminous plants by Rhizobium spp. involves a complex interaction between host plant and symbiont. Successful nodulation requires the coordinated expression of several nodulation (nod) genes in the bacteria. The expression of these genes is induced by flavonoid compounds present in root exudates of host plants. Growth of Rhizobium spp. and formation of nodules on roots of leguminous plants is known to be adversely affected by low pH and factors associated with soil acidity, but the basis of this acid-sensitivity is poorly understood. We consider that poor induction of nodulation gene expression in Rhizobium is a major factor contributing to the acid-sensitivity of nodulation formation. At low pH, induction of nod gene expression in R. leguminosarum biovar trifolii is markedly reduced in the presence of flavone-inducer. Furthermore, inducibility of nod gene expression in R. leguminosarum bv. trifolii is also affected by a net reduction in the concentration of nod gene-inducing factors present in the root exudates of clover seedlings grown in acidic conditions.

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Ramu, Senthil K., Hui-Mei Peng, and Douglas R. Cook. "Nod Factor Induction of Reactive Oxygen Species Production Is Correlated with Expression of the Early Nodulin Gene rip1 in Medicago truncatula." Molecular Plant-Microbe Interactions® 15, no. 6 (June 2002): 522–28. http://dx.doi.org/10.1094/mpmi.2002.15.6.522.

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Plant genes that are specifically activated by the rhizobial lipochitooligosaccharide signal molecule (Nod factor) in legume hosts are collectively referred to as nodulins. Although nodulin gene expression is both spatially and temporally correlated with symbiosis, the function of these genes and the molecular events underlying their expression remain unknown. Sequence analysis of rip1, an early nodulin gene encoding a putative peroxidase protein, revealed the existence of sequence motifs with homology to reactive oxygen species (ROS) responsive cis elements. Here we report that recognition of compatible Nod factor rapidly stimulates a spatially localized production of reactive oxygen species in legume roots. Sinorhizobium meliloti mutants that produce an altered Nod factor structure and a nonnodulating plant mutant, dmi1-1, that is implicated in Nod factor signal transduction are equally impaired in the ability to elicit ROS production and rip1 expression. Interestingly, both rip1 transcription and ROS production exhibit the same tissue-specific pattern of localization. Moreover, exogenous hydrogen peroxide is sufficient to activate rip1 transcription. Taken together, these results suggest that ROS production is a consequence of specific Nod factor perception and implicate H2O2 produced during this response as a mediator of Nod factor-induced rip1 expression.

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Wicker, L. S., B. J. Miller, L. Z. Coker, S. E. McNally, S. Scott, Y. Mullen, and M. C. Appel. "Genetic control of diabetes and insulitis in the nonobese diabetic (NOD) mouse." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1639–54. http://dx.doi.org/10.1084/jem.165.6.1639.

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Genetic analysis of the development of diabetes and insulitis has been performed in the nonobese diabetic (NOD) mouse strain, a model of insulin-dependent (type I) diabetes mellitus. (NOD X C57BL/10)F1, F2, and (F1 X NOD) first-, second-, and third-backcross generations were studied. The data obtained were consistent with the hypothesis that diabetes is controlled by at least three functionally recessive diabetogenic genes, or gene complexes, one of which is linked to the MHC of the NOD. In contrast, pancreatic inflammation leading to insulitis was found to be controlled by a single incompletely dominant gene. One of the two diabetogenic loci that is not linked to the MHC appears to be essential for the development of severe insulitis. This diabetogenic gene may be identical to the gene that controls the initiation of the autoimmune response that progresses to insulitis. Although this gene appears to be functionally recessive in its control of diabetes, it is incompletely dominant in its control of insulitis. The MHC-linked diabetogenic gene, although not required for the development of insulitis, apparently influences the progression of the autoimmune response since NOD MHC homozygotes in the backcross generations displayed the highest incidence and most severe cases of insulitis. Interestingly, we have found two MHC heterozygous backcross females that have become diabetic, suggesting that either the MHC-linked diabetogenic gene is not strictly recessive or that a recombination event has occurred between the diabetogenic gene and the K or I-A regions of the MHC. The third diabetogenic locus appears to influence the progression of severe insulitis to overt diabetes. In animals homozygous at this locus, diabetes may result from a decreased ability to develop a protective suppressor response to the autoimmune process.

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O'Neill, Luke. "A gene for Crohn's disease is given the nod." Trends in Pharmacological Sciences 22, no. 8 (August 2001): 398–99. http://dx.doi.org/10.1016/s0165-6147(00)01791-0.

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23

John, Michael, Jürgen Schmidt, Ursula Wieneke, Eva Kondorosi, Adam Kondorosi, and Jeff Schell. "Expression of the nodulation gene nod C of Rhizobium meliloti in Escherichia coli : role of the nod C gene product in nodulation." EMBO Journal 4, no. 10 (October 1985): 2425–30. http://dx.doi.org/10.1002/j.1460-2075.1985.tb03951.x.

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Djordjevic, MA, and JJ Weinman. "Factors Determining Host Recognition in the Clover-Rhizobium Symbiosis." Functional Plant Biology 18, no. 5 (1991): 543. http://dx.doi.org/10.1071/pp9910543.

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Rhizobia are microbes that exploit host plants as a nutritional source but cause little or no host damage. They may provide, through biological nitrogen fixation, a valuable source of nitrogen for plant growth. Different rhizobia nodulate a limited range of plants. In this review we will show that host range specificity is determined by the success or otherwise of communication events between the interacting partners. To infect different plant species, a distinct cocktail of phenolic compounds (flavonoids) is recognised. Flavonoids of the correct structure induce the expression of several bacterial nodulation (nod) and other genes required for plant infection. Flavonoids of the incorrect, but related, structure can antagonise nod gene induction. Some nod genes are responsible for the synthesis of a small family of lipo-oligosaccharides necessary for the triggering of a defined but complex series of morphological responses in the host plant including root hair curling and cortical cell division. Lipo-oligosaccharides are active at concentrations of between 10-8 and 10-12 M. The appropriate lipo-oligosaccharide required for infection of one plant host can have antagonistic effects on other non-host plants and this effect appears to be determined by minor chemical changes to the basic lipo-oligosaccharide structure. Apart from host specificity operating at the genus level, other interdependent nod gene functions determine host specificity at the cultivar level. A complex interplay between positively and negatively acting nod genes and a single host gene affects cultivar specificity in a manner analogous to, but more complex than, the gene-for-gene interactions common amongst plant-pathogen interactions.

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Madinabeitia, Nuria, Ramón A. Bellogín, Ana M. Buendía-Clavería, María Camacho, Teresa Cubo, M. Rosario Espuny, Antonio M. Gil-Serrano, et al. "Sinorhizobium fredii HH103 Has a Truncated nolO Gene Due to a -1 Frameshift Mutation That Is Conserved Among Other Geographically Distant S. fredii Strains." Molecular Plant-Microbe Interactions® 15, no. 2 (February 2002): 150–59. http://dx.doi.org/10.1094/mpmi.2002.15.2.150.

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Strain SVQ121 is a mutant derivative of Sinorhizobium fredii HH103 carrying a transposon Tn5-lacZ insertion into the nolO-coding region. Sequence analysis of the wild-type gene revealed that it is homologous to that of Rhizobium sp. NGR234, which is involved in the 3 (or 4)-O-carbamoylation of the nonreducing terminus of Nod factors. Downstream of nolO, as in Rhizobium sp. NGR234, the noeI gene responsible for methylation of the fucose moiety of Nod factors was found. SVQ121 Nod factors showed lower levels of methylation into the fucosyl residue than those of HH103, suggesting a polar effect of the transposon insertion into nolO over the noeI gene. A noeI HH103 mutant was constructed. This mutant, SVQ503, produced Nod factors devoid of methyl groups, confirming that the S. fredii noeI gene is functional. Neither the nolO nor the noeI mutation affected the ability of HH103 to nodulate several host plants, but both mutations reduced competitiveness to nodulate soybean. The Nod factors produced by strain HH103, like those of other S. fredii isolates, lack carbamoyl residues. By using specific polymerase chain reaction primers, we sequenced the nolO gene of S. fredii strains USDA192, USDA193, USDA257, and 042B(s). All the analyzed strains showed the same -1 frameshift mutation that is present in the HH103 nolO-coding region. From these results, it is concluded that, regardless of their geographical origin, S. fredii strains carry the nolO-coding region but that it is truncated by the same base-pair deletion.

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Lawson, CGR, BG Rolfe, and MA Djordjevic. "Rhizobium Inoculation Induces Condition-Dependent Changes in the Flavonoid Composition of Root Exudates From Trifolium subterraneum." Functional Plant Biology 23, no. 1 (1996): 93. http://dx.doi.org/10.1071/pp9960093.

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Rapid induction of chalcone synthase (predominantly CHSS) gene expression occurs within 6 h following the inoculation of Rhizobium leguminosarum bv. trifolii strain ANU843 on Trifolium subterraneum or wounding of plants (C. G. R. Lawson, M. A. Djordjevic, J. J. Weinman and B. G. Rolfe. 1994. Molecular Plant-Microbe Interactions 7, 498-507). Experiments were conducted under the same conditions to examine the time of onset of synthesis and excretion of flavonoids that might result from this early CHS expression. Flavonoids in root tissues and root exudates were examined by HPLC analysis and the ability of fractionated and unfractionated material to induce nodulation gene expression in Rhizobium measured. There were no detectable changes in nod-gene-inducing activity of individual HPLC fractions of root exudates of 1 day dark-grown roots after Rhizobium inoculation. In contrast, after 3 days exposure to Rhizobium, analysis of specific HPLC fractions showed the presence of an additional nod-gene-inducing compound which the data indicate was 4′,7-dihydroxyflavone. A different and additional nod gene inducer was found in inoculated 5 day samples of root exudate of light-grown plants indicating that light exposure changes the HPLC profiles as well as the nod-gene-inducing compound(s). Exudates collected from wounded plants were considerably different from those from Rhizobium-inoculated and uninoculated plants and contained no detectable nod gene inducers. The late detection (at day 3) of Rhizobium-induced flavonoid excretion may occur too late to be directly correlated with the observed expression of CHS 6 h after inoculation. In addition, the data suggest that although the CHS5 promotor responds to both wounding and Rhizobium inoculation, the biochemical consequences of CHS5 induction resulting from these treatments are different.

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Batabyal, Subrata, Sivakumar Gajjeraman, Sulagna Bhattacharya, Weldon Wright, and Samarendra Mohanty. "Nano-enhanced Optical Gene Delivery to Retinal Degenerated Mice." Current Gene Therapy 19, no. 5 (December 27, 2019): 318–29. http://dx.doi.org/10.2174/1566523219666191017114044.

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Background: The efficient and targeted delivery of genes and other impermeable therapeutic molecules into retinal cells is of immense importance for the therapy of various visual disorders. Traditional methods for gene delivery require viral transfection, or chemical methods that suffer from one or many drawbacks, such as low efficiency, lack of spatially targeted delivery, and can generally have deleterious effects, such as unexpected inflammatory responses and immunological reactions. Methods: We aim to develop a continuous wave near-infrared laser-based Nano-enhanced Optical Delivery (NOD) method for spatially controlled delivery of ambient-light-activatable Muti-Characteristic opsin-encoding genes into retina in-vivo and ex-vivo. In this method, the optical field enhancement by gold nanorods is utilized to transiently permeabilize cell membrane, enabling delivery of exogenous impermeable molecules to nanorod-binding cells in laser-irradiated regions. Results and Discussion: With viral or other non-viral (e.g. electroporation, lipofection) methods, gene is delivered everywhere, causing uncontrolled expression over the whole retina. This will cause complications in the functioning of non-degenerated areas of the retina. In the NOD method, the contrast in temperature rise in laser-irradiated nanorod-attached cells at nano-hotspots is significant enough to allow site-specific delivery of large genes. The in-vitro and in-vivo results using NOD, clearly demonstrate in-vivo gene delivery and functional cellular expression in targeted retinal regions without compromising the structural integrity of the eye or causing immune response. Conclusion: The successful delivery and expression of MCO in the targeted retina after in-vivo NOD in the mice models of retinal degeneration opens a new vista for re-photosensitizing retina with geographic atrophies, such as in dry age-related macular degeneration.

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Robinson, C. P., D. I. Bounous, C. E. Alford, K. H. Nguyen, J. M. Nanni, A. B. Peck, and M. G. Humphreys-Beher. "PSP expression in murine lacrimal glands and function as a bacteria binding protein in exocrine secretions." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 4 (April 1, 1997): G863—G871. http://dx.doi.org/10.1152/ajpgi.1997.272.4.g863.

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Nonobese diabetic (NOD) mice, an animal model for type I autoimmune diabetes and autoimmune sialoadenitis, abnormally express parotid secretory protein (PSP) in the submandibular glands (Robinson, C. P., H. Yamamoto, A. B. Peck, and M. G. Humphreys-Beher. Clin. Immunol. Immunopathol. 79: 50-59, 1996). To evaluate possible PSP gene dysregulation in the NOD mouse, we have examined a number of organs and tissues for PSP mRNA transcripts and protein expression. Results indicate that PSP is produced in the lacrimal glands of NOD mice as well as most laboratory mouse strains. Although purified salivary PSP from C3H/HeJ or BALB/c mice fails to affect amylase enzyme activity in in vitro assays, PSP bound to whole bacteria in a Zn2+-dependent manner. Additionally, radiolabeled protein bound to specific bacterial membrane proteins using a ligand binding assay. PSP gene transcription, but not protein production, was observed in the heart and pancreas from NOD mice, indicating abnormal transcription of the PSP gene. Sequence analysis of PSP cDNA from NOD mice revealed numerous base differences (compared with the published PSP sequence) capable of leading to significant amino acid substitutions, suggestive of strain-specific differences for the protein in mice. Together these results suggest that there exists in the NOD mouse a dysregulation of PSP transcription in various tissues. However, except for C3H/HeJ mice, PSP appears as a normal product of the lacrimal glands where, as in saliva, it may function as a nonimmune antimicrobial agent in the protection of tissue surfaces exposed to the external environment.

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Hubber, Andree M., John T. Sullivan, and Clive W. Ronson. "Symbiosis-Induced Cascade Regulation of the Mesorhizobium loti R7A VirB/D4 Type IV Secretion System." Molecular Plant-Microbe Interactions® 20, no. 3 (March 2007): 255–61. http://dx.doi.org/10.1094/mpmi-20-3-0255.

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The Mesorhizobium loti R7A symbiosis island contains genes encoding a VirB/D4 type IV secretion system (T4SS) similar to that of Agrobacterium tumefaciens. This system has host-dependent effects on symbiosis that probably are due to translocation of two effector proteins, Msi059 and Msi061, into host cells. Here we report that, as in A. tumefaciens, the M. loti vir genes are transcriptionally regulated by a VirA/VirG two-component regulatory system. A virGN54D mutant gene of M. loti caused constitutive expression of lacZ reporter gene fusions to virB1, virD4, msi059, and msi061. Expression of these gene fusions also was activated by a NodD gene product from Rhizobium leguminosarum in the presence of the inducer naringenin, as was a virA∷lacZ fusion. This activation was dependent on a nod box present 851 bp upstream of virA, and a mutant with the nod box deleted formed effective nodules on Leucaena leucocephala, the same symbiotic phenotype as other M.loti vir mutants. In contrast, the wild-type strain formed small, empty nodules whereas a nodD1 mutant was completely Nod¯. These results indicate that the M. loti vir genes are induced in a symbiosis-specific manner that involves a two-tiered regulatory cascade, and that the vir effectors act after Nod factor during infection thread formation.

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Schlaman, Helmi R. M., Maurien M. A. Olsthoorn, Marga Harteveld, Lucie Dörner, Michael A. Djordjevic, Jane E. Thomas-Oates, and Herman P. Spaink. "The Production of Species-Specific Highly Unsaturated Fatty Acyl-Containing LCOs from Rhizobium leguminosarum bv. trifolii Is Stringently Regulated by nodD and Involves the nodRL Genes." Molecular Plant-Microbe Interactions® 19, no. 3 (March 2006): 215–26. http://dx.doi.org/10.1094/mpmi-19-0215.

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A proportion of the Nod factors of some Rhizobium leguminosarum bv. trifolii strains is characterized by the presence of highly unsaturated fatty acyl chains containing trans double bonds in conjugation with the carbonyl group of the glycan oligosaccharide backbone. These fatty acyl chains are C18:3, C20:3, C18:4, or C20:4 and have UV-absorption maxima at 303 and 330 nm. These Nod factors are presumed to be important for host-specific nodulation on clover species. However, in wild-type R. leguminosarum bv. trifolii ANU843, Nod factors with these characteristic acyl chains were not observed using standard growth conditions. They were observed only when nod genes were present in multiple copies or when transcription was artificially increased to higher levels by introduction of extra copies of the transcriptional regulator gene nodD. In a screen for the genetic requirements for production of the Nod factors with these characteristic structures, it was found that the region downstream of nodF and nodE is essential for the presence of highly unsaturated fatty acyl moieties. Mu-lacZ insertion in this region produced a mutant that did not produce detectable levels of the highly unsaturated fatty acyl-bearing Nod factors. The Mu-lacZ insertion was translationally fused to a putative new gene, designated nodR, in the nodE-nodL intergenic region; however, no predicted function for the putative NodR protein has been obtained from data-base homology searches. In a set of 12 wild-type strains of R. leguminosarum bv. trifolii originating from various geographical regions that were analyzed for the presence of a nodR-like gene, it was found that seven strains carry a homologous NodR open reading frame. Taken together, our results suggest a tightly controlled regulation of nod genes, in which we propose that it is the balance of transcriptional levels of nodFE and the nodRL genes that is critical for determining the presence of highly unsaturated fatty acyl moieties in the Nod factors produced by R. leguminosarum bv. trifolii.

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Yokoyama, Tadashi, Norihiko Tomooka, Masanori Okabayashi, Akito Kaga, Nantakorn Boonkerd, and Duncan A. Vaughan. "Variation in the nod gene RFLPs, nucleotide sequences of 16S rRNA genes, Nod factors, and nodulation abilities of Bradyrhizobium strains isolated from Thai Vigna plants." Canadian Journal of Microbiology 52, no. 1 (January 1, 2006): 31–46. http://dx.doi.org/10.1139/w05-099.

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The analysis of nod genes and 16S rRNA gene regions, Nod factors, and nodulation abilities of Brady rhizobium strains isolated from tropical Thai Vigna species is reported. A total of 55 Bradyrhizobium strains isolated from two cultivated and six wild Vigna species growing in central and northern Thailand were evaluated. Thai Vigna spp. Bradyrhizobium strains showed higher levels of nod gene RFLP diversity compared with Thai soybean Brady rhizobium strains or temperate strains of Bradyrhizobium japonicum and Bradyrhizobium elkanii. Analysis of the 16S rRNA gene region using selected strains also suggests a high genetic diversity of the Thai Vigna–Bradyrhizobium association. Based on thin-layer chromatography analysis, Nod factors produced by tropical Thai Vigna spp. Brady rhizobium strains are more diverse than temperate Japanese and US strains of B. japonicum and B. elkanii. Thai Vigna spp. Bradyrhizobium strains showed variation in nodulation ability and affinity, estimated by the number of normal nodules versus green nodules in an inoculation study. There are some Bradyrhizobium–host combinations that could not form any nodules, suggesting that some genetic differentiation has evolved in their host range. However, most of the Thai Vigna spp. Bradyrhizobium strains formed nodules on the cultigens soybean (Glycine max), mungbean (Vigna radiata), azuki bean (Vigna angularis), and cowpea (Vigna unguiculata). This is the first study on Bradyrhizobium strains associated with a range of cultivated and wild Vigna and reveals that these Bradyrhizobium strains are diverse and may provide novel sources of useful variation for the improvement of symbiotic systems.Key words: Bradyrhizobium, Vigna, common nod gene, 16S rRNA genes, RFLP, Thailand.

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Ikeda, Seishi, Mizue Anda, Shoko Inaba, Shima Eda, Shusei Sato, Kazuhiro Sasaki, Satoshi Tabata, et al. "Autoregulation of Nodulation Interferes with Impacts of Nitrogen Fertilization Levels on the Leaf-Associated Bacterial Community in Soybeans." Applied and Environmental Microbiology 77, no. 6 (January 14, 2011): 1973–80. http://dx.doi.org/10.1128/aem.02567-10.

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ABSTRACTThe diversities leaf-associated bacteria on nonnodulated (Nod−), wild-type nodulated (Nod+), and hypernodulated (Nod++) soybeans were evaluated by clone library analyses of the 16S rRNA gene. To analyze the impact of nitrogen fertilization on the bacterial leaf community, soybeans were treated with standard nitrogen (SN) (15 kg N ha−1) or heavy nitrogen (HN) (615 kg N ha−1) fertilization. Under SN fertilization, the relative abundance ofAlphaproteobacteriawas significantly higher in Nod−and Nod++soybeans (82% to 96%) than in Nod+soybeans (54%). The community structure of leaf-associated bacteria in Nod+soybeans was almost unaffected by the levels of nitrogen fertilization. However, differences were visible in Nod−and Nod++soybeans. HN fertilization drastically decreased the relative abundance ofAlphaproteobacteriain Nod−and Nod++soybeans (46% to 76%) and, conversely, increased those ofGammaproteobacteriaandFirmicutesin these mutant soybeans. In theAlphaproteobacteria, cluster analyses identified two operational taxonomic units (OTUs) (Aurantimonassp. andMethylobacteriumsp.) that were especially sensitive to nodulation phenotypes under SN fertilization and to nitrogen fertilization levels. Arbuscular mycorrhizal infection was not observed on the root tissues examined, presumably due to the rotation of paddy and upland fields. These results suggest that a subpopulation of leaf-associated bacteria in wild-type Nod+soybeans is controlled in similar ways through the systemic regulation of autoregulation of nodulation, which interferes with the impacts of N levels on the bacterial community of soybean leaves.

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Chen, Wen-Ming, Lionel Moulin, Cyril Bontemps, Peter Vandamme, Gilles Béna, and Catherine Boivin-Masson. "Legume Symbiotic Nitrogen Fixation byβ-Proteobacteria Is Widespread inNature." Journal of Bacteriology 185, no. 24 (December 15, 2003): 7266–72. http://dx.doi.org/10.1128/jb.185.24.7266-7272.2003.

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ABSTRACT Following the initial discovery of two legume-nodulating Burkholderia strains (L. Moulin, A. Munive, B. Dreyfus, and C. Boivin-Masson, Nature 411:948-950, 2001), we identified as nitrogen-fixing legume symbionts at least 50 different strains of Burkholderia caribensis and Ralstonia taiwanensis, all belonging to the β-subclass of proteobacteria, thus extending the phylogenetic diversity of the rhizobia. R. taiwanensis was found to represent 93% of the Mimosa isolates in Taiwan, indicating thatβ -proteobacteria can be the specific symbionts of a legume. The nod genes of rhizobial β-proteobacteria (β-rhizobia) are very similar to those of rhizobia from theα -subclass (α-rhizobia), strongly supporting the hypothesis of the unique origin of common nod genes. Theβ -rhizobial nod genes are located on a 0.5-Mb plasmid, together with the nifH gene, in R. taiwanensis and Burkholderia phymatum. Phylogenetic analysis of available nodA gene sequences clustered β-rhizobial sequences in two nodA lineages intertwined with α-rhizobial sequences. On the other hand, theβ -rhizobia were grouped with free-living nitrogen-fixingβ -proteobacteria on the basis of the nifH phylogenetic tree. These findings suggest that β-rhizobia evolved from diazotrophs through multiple lateral nod gene transfers.

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Wieczorek, Grazyna, Marc Bigaud, Sabina Pfister, Melanie Ceci, Katriona McMichael, Catherine Afatsawo, Meike Hamburger, et al. "Blockade of CD40–CD154 pathway interactions suppresses ectopic lymphoid structures and inhibits pathology in the NOD/ShiLtJ mouse model of Sjögren’s syndrome." Annals of the Rheumatic Diseases 78, no. 7 (March 22, 2019): 974–78. http://dx.doi.org/10.1136/annrheumdis-2018-213929.

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ObjectiveTo examine the role of CD40–CD154 costimulation and effects of therapeutic pathway blockade in the non-obese diabetic (NOD/ShiLtJ) model of Sjögren’s syndrome (SS).MethodsWe assessed leucocyte infiltration in salivary glands (SGs) from NOD/ShiLtJ mice by immunohistochemistry and examined transcriptomics data of SG tissue from these animals for evidence of a CD40 pathway gene signature. Additionally, we dosed MR1 (anti-CD154 antibody) in NOD mice after the onset of SS-like disease and examined the effects of MR1 treatment on sialadenitis, autoantibody production, SG leucocyte infiltration, gene expression downstream of CD40 and acquaporin 5 (AQP5) expression.ResultsWe could detect evidence of CD40 expression and pathway activation in SG tissue from NOD mice. Additionally, therapeutic treatment with MR1 suppressed CD40 pathway genes and sialadenitis, inhibited ectopic lymphoid structure formation and autoantibody production, as well as decreased the frequency of antibody-secreting cells in SGs but had minimal effects on AQP5 expression in NOD/ShiLtJ SGs.ConclusionCD40–CD154 interactions play an important role in key pathological processes in a mouse model of SS, suggesting that blockade of this costimulatory pathway in the clinic may have beneficial therapeutic effects in patients suffering from this autoimmune exocrinopathy.

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Gagnon, Hubert, and Ragai K. Ibrahim. "Aldonic Acids: A Novel Family of nod Gene Inducers of Mesorhizobium loti, Rhizobium lupini, and Sinorhizobium meliloti." Molecular Plant-Microbe Interactions® 11, no. 10 (October 1998): 988–98. http://dx.doi.org/10.1094/mpmi.1998.11.10.988.

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Molecular signals, such as flavonoids (or nonflavonoid type), nod gene-inducers, and bacterial lipochitin oligosac-charides (LCOs) act as modulators of species specificity during early stages of infection in Rhizobium spp.-legume interactions. The fact that signaling in Lupinus albus remains to be determined prompted us to investigate the flavonoid signal responsible for nod gene induction in Rhizobium lupini. A screening method was used based on the measurement of β-galactosidase activity of R. lupini strains harboring nodC::lacZ fusions in the presence of (i) authentic lupin isoflavones, (ii) carbohydrate-like inducers, and (iii) high-pressure liquid chromatography (HPLC)-fractionated lupin seed effusates and root exudates, as putative nod gene inducers. The results indicate that both erythronic and tetronic acids (4-C sugar acids) led to low but significant increases in β-galactosidase activities, compared with the controls. In addition, lupi-wighteone, a monoprenylated isoflavone, exerts a synergistic effect with the carbohydrate-like inducers, compared with other isoflavone treatments. The natural occurrence of aldonic acids in L. albus root exudates and seed effusates has been demonstrated by HPLC analysis. When tested with nodC::lacZ fusions, tetronic acid resulted in nod gene induction in Sinorhizobium meliloti. In addition, a combination of luteolin and tetronic acid promotes further increases in S. meliloti nod gene expression, as shown by β-galactosidase assays. Incorporation studies with [14C]LCO precursors confirmed the inductive role of both erythronic and tetronic acids in promoting LCO biosynthesis in R. lupini cultures, and of tetronic acid in Mesorhizobium loti and S. meliloti. Hydrolysis of the LCOs with various enzymes substantiated their putative identities. These results are discussed in relation to the impact of these unusual signal molecules on our knowledge of flavonoid signaling in Rhizobium-legume symbiosis.

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Ip, H., F. D'Aoust, A. A. Begum, H. Zhang, D. L. Smith, B. T. Driscoll, and T. C. Charles. "Bradyrhizobium japonicum Mutants with Enhanced Sensitivity to Genistein Resulting in Altered nod Gene Regulation." Molecular Plant-Microbe Interactions® 14, no. 12 (December 2001): 1404–10. http://dx.doi.org/10.1094/mpmi.2001.14.12.1404.

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Bradyrhizobium japonicum mutants with altered nod gene induction characteristics were isolated by screening mutants for genistein-independent nod gene expression. Plasmid pZB32, carrying a nodY∷lacZ transcriptional gene fusion, was introduced into B. japonicum cells that had been subjected to UV mutagenesis. Ten independent transformants producing a blue color on plates containing 5-bromo-4chloro-3indolyl-β-d-galactopyranoside but lacking genistein, indicative of constitutive expression of the nodY∷lacZ reporter gene, were isolated. β-Galactosidase activity assays revealed that while all of the 10 strains were sensitive to low concentrations of genistein, none exhibited truly constitutive nodY∷lacZ expression in liquid culture. Soybean plants inoculated with three of the mutants were chlorotic and stunted, with shoot dry weights close to those of the uninoculated plants, indicating the absence of nitrogen fixation. Differences in the kinetics of nodY∷lacZ expression and lipochitin oligosaccharide Nod signal production suggested that the strains carried different mutations. Some of these strains may be useful in mitigating the low root zone temperature-associated delay in soybean nodulation at the northern extent of soybean cultivation.

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Fisher, Robert F., Jean A. Swanson, John T. Mulligan, and Sharon R. Long. "Extended Region of Nodulation Genes in Rhizobium meliloti 1021. II. Nucleotide Sequence, Transcription Start Sites and Protein Products." Genetics 117, no. 2 (October 1, 1987): 191–201. http://dx.doi.org/10.1093/genetics/117.2.191.

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ABSTRACT We have established the DNA sequence and analyzed the transcription and translation products of a series of putative nodulation (nod) genes in Rhizobium meliloti strain 1021. Four loci have been designated nodF, nodE, nodG and nodH. The correlation of transposon insertion positions with phenotypes and open reading frames was confirmed by sequencing the insertion junctions of the transposons. The protein products of these nod genes were visualized by in vitro expression of cloned DNA segments in a R. meliloti transcription-translation system. In addition, the sequence for nodG was substantiated by creating translational fusions in all three reading frames at several points in the sequence; the resulting fusions were expressed in vitro in both E. coli and R. meliloti transcription-translation systems. A DNA segment bearing several open reading frames downstream of nodG corresponds to the putative nod gene mutated in strain nod-216. The transcription start sites of nodF and nodH were mapped by primer extension of RNA from cells induced with the plant flavone, luteolin. Initiation of transcription occurs approximately 25 bp downstream from the conserved sequence designated the "nod box," suggesting that this conserved sequence acts as an upstream regulator of inducible nod gene expression. Its distance from the transcription start site is more suggestive of an activator binding site rather than an RNA polymerase binding site.

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Horn, Peter A., Bobbie M. Thomasson, Brent L. Wood, Robert G. Andrews, Julia C. Morris, and Hans-Peter Kiem. "Distinct hematopoietic stem/progenitor cell populations are responsible for repopulating NOD/SCID mice compared with nonhuman primates." Blood 102, no. 13 (December 15, 2003): 4329–35. http://dx.doi.org/10.1182/blood-2003-01-0082.

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AbstractThe nonobese diabetic/severe combined immune-deficient (NOD/SCID) mouse xenotransplantation assay is the most commonly used surrogate assay for the study of human candidate stem cells. In contrast to large animal and human studies, however, it is limited by the short life span of the recipients, the limited proliferative demand placed on the transplanted cells, and the inability to support differentiation into all hematopoietic lineages. In the present study, we directly compared hematopoietic repopulation in NOD/SCID mice with autologous reconstitution in the baboon, a well-established preclinical large animal model for stem cell transplantation. Baboon CD34-enriched marrow cells were retrovirally marked and infused into the irradiated baboon and the NOD/SCID mice. Although the percentage of gene-marked cells was high and remained stable in NOD/SCID mice up to 12 weeks and in those that underwent secondary transplantation, we observed a considerable decline and overall a significantly (10-fold) lower percentage of gene-marked cells in the baboons. In addition, clonal integration site analysis revealed common proviral vector integrants in NOD/SCID repopulating cells and in the baboon at 6 weeks but not at 6 months after transplantation. These results suggest that distinct hematopoietic stem/progenitor cells are responsible for hematopoietic reconstitution in NOD/SCID mice compared with nonhuman primates. (Blood. 2003;102:4329-4335)

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Serreze, D. V., M. Prochazka, P. C. Reifsnyder, M. M. Bridgett, and E. H. Leiter. "Use of recombinant congenic and congenic strains of NOD mice to identify a new insulin-dependent diabetes resistance gene." Journal of Experimental Medicine 180, no. 4 (October 1, 1994): 1553–58. http://dx.doi.org/10.1084/jem.180.4.1553.

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Insulin-dependent diabetes mellitus (IDDM) in NOD/Lt mice represents a complex polygenic disease. NOR/Lt is a recombinant congenic strain (RCS) in which limited regions of the NOD/Lt genome have been replaced by genome from the C57BL/KsJ strain. NOR mice are insulitis resistant and diabetes free despite genetic identity with NOD at numerous chromosomal regions containing previously described insulin-dependent diabetes (Idd) genes, including the strongly diabetogenic H2g7 major histocompatibility complex (MHC) haplotype. The present study revealed BKs-derived genome on segments of chromosomes (Chr) 1, 2, 4, 5, 7, 11, 12, and 18, approximating 11.6% of the total NOR genome analyzed. (NOD x NOR)F2 segregation analysis was employed to identify chromosomal regions in NOR containing Idd resistance alleles. IDDM developed in 33% (10/30) of F1 females, and 29.3% (36/123) of F2 females aged to 1 yr. A previously unrecognized diabetes resistance locus (designated Idd13r) strongly protective in homozygous state was identified on NOR Chr 2 in linkage with the Il1 alpha structural gene. The existence of this locus was confirmed by construction of a NOD stock congenic for NOR-derived markers on Chr 2. Our analysis shows the utility of RCS and congenic stocks for the identification and isolation of non-MHC genes with strong antidiabetogenic functions.

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Tsyganov, Viktor E., Vera A. Voroshilova, Sergey M. Rozov, Aleksey U. Borisov, and Igor A. Tikhonovich. "Novel series os pea symbiotic mutants induced in the SGE line." Ecological genetics 10, no. 1 (March 15, 2012): 19–26. http://dx.doi.org/10.17816/ecogen10119-26.

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Using ethylmethansulphonate the chemical mutagenesis of the pea laboratory line SGE was performed. During analysis of 425 families (2069 plants) of М2 progeny 45 putative mutants were selected, among them 30 mutants forming ineffective nodules (Fix– phenotype), 13 mutantsunable to form nodules (Nod– phenotype), and 2 mutants forming a few nodules (Nod+/– phenotype). For 1 Nod– and 5 Fix– mutants monogenic inheritance and recessive phenotype manifestation were demonstrated. For Fix– mutant SGEFix––9 an additional mutation leading to Nod+/– phenotype was shown. Complementation analysis showed that the mutant phenotype of the SGEFix- - 5 line is caused by a mutation in the sym33 gene, of theSGEFix––6 linein the sym40 gene, of the SGEFix––7 line in the sym27 gene, and of the SGEFix––8 linein the sym25 gene.

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Yokoyama, Tadashi. "Flavonoid-responsive nodY-lacZ expression in three phylogenetically different Bradyrhizobium groups." Canadian Journal of Microbiology 54, no. 5 (May 2008): 401–10. http://dx.doi.org/10.1139/w08-021.

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Previously, restriction fragment length polymorphism analysis using the nodD1YABC gene probe showed the genetic diversity of common nodD1ABC gene regions of Bradyrhizobium japonicum , Bradyrhizobium elkanii , and the Thai soybean Bradyrhizobium. The nodD1 sequences of representative strains of the 3 groups differed phylogenetically, suggesting that responses of NodD1 proteins of the 3 Bradyrhizobium groups to diverse flavonoids may differ. To confirm this hypothesis, 6 representative strains were chosen from the 3 Bradyrhizobium groups. Six reporter strains were constructed, all carrying the pZB32 plasmid, which contains a nod box and the nodY-lacZ fusion of B. japonicum USDA 110. Differences in nodY-lacZ expression among the strains in response to 37 flavonoid compounds at various concentrations were evaluated. Of those compounds, prunetin (4′,5-dihydroxy-7-methoxyisoflavone) and esculetin (6,7-dihydroxycoumarin) were identified as Bradyrhizobium group-specific nod gene inducers. Esculetin showed nod gene induction activities unique to Thai Bradyrhizobium strains. The levels of nodY-lacZ induction among B. japonicum and Thai Bradyrhizobium strains increased with increasing concentration of prunetin, whereas, those in B. elkanii strains did not.

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Corvera, Adriana, Danielle Promé, Jean-Claude Promé, Esperanza Martínez-Romero, and David Romero. "The nolL Gene from Rhizobium etli Determines Nodulation Efficiency by Mediating the Acetylation of the Fucosyl Residue in the Nodulation Factor." Molecular Plant-Microbe Interactions® 12, no. 3 (March 1999): 236–46. http://dx.doi.org/10.1094/mpmi.1999.12.3.236.

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The nodulation factors (Nod factors) of Rhizobium etli and R. loti carry a 4-O-acetyl-L-fucosyl group at the reducing end. It has been claimed, based on sequence analysis, that NolL from R. loti participates in the 4-O-acetylation of the fucosyl residue of the Nod factors, as an acetyl-transferase (D. B. Scott, C. A. Young, J. M. Collins-Emerson, E. A. Terzaghi, E. S. Rockman, P. A. Lewis, and C. E. Pankhurst. Mol. Plant-Microbe Interact. 9:187–197, 1996). Further support for this hypothesis was obtained by studying the production of Nod factors in an R. etli nolL::Km mutant. Chromatographic and mass spectrometry analysis of the Nod factors produced by this strain showed that they lack the acetyl-fucosyl substituent, having a fucosyl group instead. Acetyl-fucosylation was restored upon complementation with a wild-type nolL gene. These results indicate that the nolL gene determines 4-O-acetylation of the fucosyl residue in Nod factors. Analysis of the predicted NolL polypeptide suggests a transmembranal location and that it belongs to the family of integral membrane transacylases (J. M. Slauch, A. A. Lee, M. J. Mahan, and J. J. Mekalanos. J. Bacteriol. 178:5904–5909, 1996). NolL from R. loti was also proposed to function as a transporter; our results show that NolL does not determine a differential secretion of Nod factors from the cell. We also performed plant assays that indicate that acetylation of the fucose conditions efficient nodulation by R. etli of some Phaseolus vulgaris cultivars, as well as of an alternate host (Vigna umbellata).

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Rumore-Maton, B., J. Elf, N. Belkin, B. Stutevoss, F. Seydel, E. Garrigan, and S. A. Litherland. "M-CSF and GM-CSF Regulation of STAT5 Activation and DNA Binding in Myeloid Cell Differentiation is Disrupted in Nonobese Diabetic Mice." Clinical and Developmental Immunology 2008 (2008): 1–8. http://dx.doi.org/10.1155/2008/769795.

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Defects in macrophage colony-stimulating factor (M-CSF) signaling disrupt myeloid cell differentiation in nonobese diabetic (NOD) mice, blocking myeloid maturation into tolerogenic antigen-presenting cells (APCs). In the absence of M-CSF signaling, NOD myeloid cells have abnormally high granulocyte macrophage colony-stimulating factor (GM-CSF) expression, and as a result, persistent activation of signal transducer/activator of transcription 5 (STAT5). Persistent STAT5 phosphorylation found in NOD macrophages is not affected by inhibiting GM-CSF. However, STAT5 phosphorylation in NOD bone marrow cells is diminished if GM-CSF signaling is blocked. Moreover, if M-CSF signaling is inhibited, GM-CSF stimulationin vitrocan promote STAT5 phosphorylation in nonautoimmune C57BL/6 mouse bone marrow cultures to levels seen in the NOD. These findings suggest that excessive GM-CSF production in the NOD bone marrow may interfere with the temporal sequence of GM-CSF and M-CSF signaling needed to mediate normal STAT5 function in myeloid cell differentiation gene regulation.

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Chen, Y. G., M. H. Forsberg, S. Khaja, A. E. Ciecko, M. J. Hessner, and A. M. Geurts. "Gene Targeting in NOD Mouse Embryos Using Zinc-Finger Nucleases." Diabetes 63, no. 1 (August 23, 2013): 68–74. http://dx.doi.org/10.2337/db13-0192.

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Roca-Ho, Heleia, Marta Riera, Marta Rebull, Julio Pascual, and Mª José Soler. "FP464DELETION OF ACE2 GENE IMPAIRS GLUCOSE HOMEOSTASIS IN NOD MICE." Nephrology Dialysis Transplantation 30, suppl_3 (May 2015): iii226. http://dx.doi.org/10.1093/ndt/gfv178.24.

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Shizuru, J. A., C. Taylor-Edwards, A. Livingstone, and C. G. Fathman. "Genetic dissection of T cell receptor V beta gene requirements for spontaneous murine diabetes." Journal of Experimental Medicine 174, no. 3 (September 1, 1991): 633–38. http://dx.doi.org/10.1084/jem.174.3.633.

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It has been demonstrated, in certain autoimmune disease models, that pathogenic T cells express antigen receptors of limited diversity. It has been suggested that the T cells responsible for the pathogenesis of type I diabetes mellitus might similarly demonstrate restricted T cell receptor (TCR) usage. Recently, attempts have been made to identify the V beta subset(s) that initiates and/or perpetuates the antiislet response in a mouse model of spontaneous autoimmune diabetes (non-obese diabetic [NOD] mice). In studies reported here, we have bred NOD mice to a mouse strain that congenitally lacks approximately one-half of the conventional TCR V beta alleles. Included in this deletion are TCR V beta gene products previously implicated as being involved in the pathogenesis of NOD disease. By studying second backcross-intercross animals, we were able to demonstrate that this deletion of TCR V beta gene segments did not prevent the development of insulitis or diabetes.

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47

Schiedlmeier, B., K. Kühlcke, H. G. Eckert, C. Baum, W. J. Zeller, and S. Fruehauf. "Quantitative assessment of retroviral transfer of the human multidrug resistance 1 gene to human mobilized peripheral blood progenitor cells engrafted in nonobese diabetic/severe combined immunodeficient mice." Blood 95, no. 4 (February 15, 2000): 1237–48. http://dx.doi.org/10.1182/blood.v95.4.1237.

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Mobilized peripheral blood progenitor cells (PBPC) are a potential target for the retrovirus-mediated transfer of cytostatic drug-resistance genes. We analyzed nonobese diabetic/severe combined immunodeficient (NOD/SCID) mouse-repopulating CD34+ PBPC from patients with cancer after retroviral transduction in various cytokine combinations with the hybrid vector SF-MDR, which is based on the Friend mink cell focus-forming/murine embryonic stem-cell virus and carries the human multidrug resistance 1 (MDR1) gene. Five to 13 weeks after transplantation of CD34+ PBPC into NOD/SCID mice (n = 84), a cell dose-dependent multilineage engraftment of human leukocytes up to an average of 33% was observed. The SF-MDR provirus was detected in the bone marrow (BM) and in its granulocyte fractions in 96% and 72%, respectively, of chimeric NOD/SCID mice. SF-MDR provirus integration assessed by quantitative real-time polymerase chain reaction (PCR) was optimal in the presence of Flt-3 ligand/thrombopoietin/stem-cell factor, resulting in a 6-fold (24% ± 5% [mean ± SE]) higher average proportion of gene-marked human cells in NOD/SCID mice than that achieved with IL-3 alone (P < .01). A population of clearly rhodamine-123dull human myeloid progeny cells could be isolated from BM samples from chimeric NOD/SCID mice. On the basis of PCR and rhodamine-123 efflux data, up to 18% ± 4% of transduced cells were calculated to express the transgene. Our data suggest that the NOD/SCID model provides a valid assay for estimating the gene-transfer efficiency to repopulating human PBPC that may be achievable in clinical autologous transplantation. P-glycoprotein expression sufficient to prevent marrow aplasia in vivo may be obtained with this SF-MDR vector and an optimized transduction protocol.

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López, Juan Carlos, Daniel H. Grasso, Florian Frugier, Martín D. Crespi, and O. Mario Aguilar. "Early Symbiotic Responses Induced by Sinorhizobium meliloti ilvC Mutants in Alfalfa." Molecular Plant-Microbe Interactions® 14, no. 1 (January 2001): 55–62. http://dx.doi.org/10.1094/mpmi.2001.14.1.55.

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A mutation in the ilvC gene of Sinorhizobium meliloti 1021 determines a symbiotically defective phenotype. ilvC mutants obtained from different S. meliloti wild-type strains are able to induce root hair deformation on alfalfa roots and show variable activation of the common nodulation genes nodABC. All of these mutants are noninfective. The presence of extra copies of nodD3-syrM in an IlvC¯ background does not promote nod expression but allows the detection of low levels of Nod factor production. The sulphation of the Nod factor metabolites, however, is not affected. Furthermore, IlvC¯ strains induce a specific pattern of starch accumulation on alfalfa roots as well as of early nodulin expression. Hence, the pleiotropic action of the ilvC gene in S. meliloti may reveal novel complexities involved in the symbiotic interaction.

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Barran, L. R., and E. S. P. Bromfield. "Symbiotic gene probes hybridize to cryptic plasmids of indigenous Rhizobium meliloti." Canadian Journal of Microbiology 34, no. 5 (May 1, 1988): 703–7. http://dx.doi.org/10.1139/m88-119.

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DNA probes for host specific nodulation (hsn) common nodulation (nod), exopolysaccharide (exo), nodule development (ndv) and nitrogenase structural (nif) genes were used to examine a collection of symbiotically effective, genotypically distinct isolates of indigenous Rhizobium meliloti for reiteration of symbiotic DNA sequences on cryptic plasmids. Nineteen of 30 isolates possessed at least one cryptic plasmid with reiterated DNA sequences, and of these isolates 15, 5, and 1 contained cryptic plasmids that hybridized to hsn, nif, and nod gene probes respectively; both hsn and nif probes hybridized to a single cryptic plasmid in each of two isolates. The exo and ndv probes did not hybridize to cryptic plasmids in any of the 30 isolates of R. meliloti.

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Kondorosi, A., E. Kondorosi, Z. Györgypal, Z. Banfalvi, J. Gyuris, P. Putnoky, E. Grosskopf, et al. "Molecular genetic basis of Rhizobium–legume interactions." Genome 31, no. 1 (January 1, 1989): 350–53. http://dx.doi.org/10.1139/g89-053.

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Recognition of the appropriate legume and nodule induction are controlled by common (nod) and host-specific nodulation (hsn) genes in Rhizobium. The nod and hsn genes are activated by the product of the regulatory nodD in conjunction with specific flavonoids excreted by the plant. Differences in the flavonoid specificity of the NodD proteins occur between different Rhizobium species, or between strains of a given species or even within one strain containing several copies of the nodD gene. Accordingly, the nodD gene controls the host-specific expression of nod and hsn genes. In addition, the nodulation genes are under not only positive but also negative regulation which is mediated by a nod-specific repressor protein. This dual control is required for optimal nodulation of the plant host. Further steps in nodule development are again controlled by the infecting Rhizobium. It was found that at least four different classes of Rhizobium fix genes are involved directly or indirectly in the expression of late nodulin genes, finally leading to the establishment of nitrogen-fixing symbiosis.Key words: Rhizobium meliloti, nodulation genes, plant signals, fix genes, alfalfa.

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Journal articles on the topic 'Gene nod'

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