Repression of the auxin response pathway increases Arabidopsis susceptibility to necrotrophic fungi

In plants, resistance to necrotrophic pathogens depends on the interplay between different hormone systems, such as those regulated by salicylic acid (SA), jasmonic acid (JA), ethylene, and abscisic acid. Repression of auxin signaling by the SA pathway was recently shown to contribute to antibacterial resistance. Here, we demonstrate that Arabidopsis auxin signaling mutants axr1, axr2, and axr6 that have defects in the auxin-stimulated SCF (Skp1¿Cullin¿ F-box) ubiquitination pathway exhibit increased susceptibility to the necrotrophic fungi Plectosphaerella cucumerina and Botrytis cinerea. Also, stabilization of the auxin transcriptional repressor AXR3 that is normally targeted for removal by the SCF-ubiquitin/proteasome machinery occurs upon P. cucumerina infection. Pharmacological inhibition of auxin transport or proteasome function each compromise necrotroph resistance of wild-type plants to a similar extent as in non-treated auxin response mutants. These results suggest that auxin signaling is important for resistance to the necrotrophic fungi P. cucumerina and B. cinerea. SGT1b (one of two Arabidopsis SGT1 genes encoding HSP90/HSC70 co-chaperones) promotes the functions of SCF E3-ubiquitin ligase complexes in auxin and JA responses and resistance conditioned by certain Resistance (R) genes to biotrophic pathogens. We find that sgt1b mutants are as resistant to P. cucumerina as wild-type plants. Conversely, auxin/SCF signaling mutants are uncompromised in RPP4-triggered resistance to the obligate biotrophic oomycete, Hyaloperonospora parasitica. Thus, the predominant action of SGT1b in R gene-conditioned resistance to oomycetes appears to be at a site other than assisting SCF E3-ubiquitin ligases. However, genetic additivity of sgt1b axr1 double mutants in susceptibility to H. parasitica suggests that SCF-mediated ubiquitination contributes to limiting biotrophic pathogen colonization once plant¿pathogen compatibility is established

Adherence to behavioural interventions in multiple sclerosis: Follow-up meeting report (AD@MS-2)

After an initial meeting in 2013 that reviewed adherence to disease modifying therapy, the AD@MS group conducted a follow-up meeting in 2014 that examined adherence to behavioural interventions in MS (e.g. physical activity, diet, psychosocial interventions). Very few studies have studied adherence to behavioural interventions in MS. Outcomes beyond six months are lacking, as well as implementation work in the community. Psychological interventions need to overcome stigma and other barriers to facilitate initiation and maintenance of behaviour change. A focus group concentrated on physical activity and exercise as one major behavioural intervention domain in MS. The discussion revealed that patients are confronted with multiple challenges when attempting to regularly engage in physical activity. Highlighted needs for future research included an improved understanding of patients’ and health experts’ knowledge and attitudes towards physical activity as well as a need for longitudinal research that investigates exercise persistence

The relationship between processing speed and verbal and non-verbal new learning and memory in progressive multiple sclerosis

Objective: Processing speed (PS) deficits are the most common cognitive deficits in multiple sclerosis (MS), followed by learning and memory deficits, and are often an early cognitive problem. It has been argued that impaired PS is a primary consequence of MS, which in turn decreases learning. The current analysis examined the association between PS and learning in a large cohort of individuals with progressive MS. Methods: Baseline data from a randomized clinical trial on rehabilitation taking place at 11 centers across North America and Europe were analyzed. Participants included 275 individuals with clinically definite progressive MS (primary, secondary) consented into the trial. Results: Symbol Digit Modalities Test (SDMT) significantly correlated with California Verbal Learning Test-II (CVLT-II) (r = 0.21, p = 0.0003) and Brief Visuospatial Memory Test–Revised (BVMT-R) (r = 0.516, p < 0.0001). Receiver operating characteristic (ROC) analysis of the SDMT z score to distinguish between impaired and non-impaired CVLT-II performance demonstrated an area under the curve (AUC) of 0.61 (95% confidence interval (CI): 0.55–0.68) and a threshold of −1.62. ROC analysis between SDMT and BVMT-R resulted in an AUC of 0.77 (95% CI: 0.71–0.83) and threshold of −1.75 for the SDMT z score to predict impaired BVMT-R. Conclusion: Results indicate little ability beyond chance to predict CVLT-II from SDMT (61%), albeit statistically significant. In contrast, there was a 77% chance that the model could distinguish between impaired and non-impaired BVMT-R. Several potential explanations are discussed

Late orogenic carboniferous extensions in the Variscan French Massif Central

International audienceThe Variscan French Massif Central experienced two successive stages of extension from Middle Carboniferous to Early Permian. In the northern Massif Central, the first stage began in the late Visean, immediately after nappe stacking, and is well recorded by Namurian-Westphalian synkinematic plutonism. The Middle Carboniferous leucogranites widespread in the NW Massif Central (Limousin and Sioule area) were emplaced within a crust extending along a NE-SW direction. At the same time, the hanging wall or "Guéret extensional allochton" moved toward the SE. Several examples of the synextensional plutonism are also recognized in central Limousin: Saint Mathieu dome, La Porcherie, and Cornil leucogranites. These examples illustrate the relationship between granite emplacement and crustal scale deformation characterized by NW-SE stretching and NE-SW shortening. In the central and southern Massif Central (Cévennes, Châtaigneraie, and Margeride areas), plutonism is dominantly granodioritic and exhibits the same structural features: NW-SE maximum stretching and overturning to the SE. Middle Carboniferous (Namurian-Westphalian) extension was parallel to the Variscan belt both in the Massif Central and southern Armorican area. This extensional regime was active from the late Visean in the north, while compression dominated in the southernmost domains (Montagne Noire and Pyrenées). The second extensional stage occurred from Late Carboniferous to Early Permian. This event was responsible for the opening of intramontane coal basins, brittle deformation in the upper crust, and ductile normal faulting localized on the margin of cordierite granite-migmatite domes. Data from the coal basins show that the half-graben is the dominant structural style, except for basins located along submeridianal left-lateral faults which have pull-apart geometries. Late Carboniferous extension occurred along the NE-SW direction. The NE-SW maximum stretching direction can be found in the whole Massif Central but is more developed in the eastern part. The extensional direction is transverse to the general trend of the belt, and top-to-the-NE shearing is dominant. Correlations of these two extension directions with neighboring Variscan massifs are discussed

Two-Component Elements Mediate Interactions between Cytokinin and Salicylic Acid in Plant Immunity

Recent studies have revealed an important role for hormones in plant immunity. We are now beginning to understand the contribution of crosstalk among different hormone signaling networks to the outcome of plant–pathogen interactions. Cytokinins are plant hormones that regulate development and responses to the environment. Cytokinin signaling involves a phosphorelay circuitry similar to two-component systems used by bacteria and fungi to perceive and react to various environmental stimuli. In this study, we asked whether cytokinin and components of cytokinin signaling contribute to plant immunity. We demonstrate that cytokinin levels in Arabidopsis are important in determining the amplitude of immune responses, ultimately influencing the outcome of plant–pathogen interactions. We show that high concentrations of cytokinin lead to increased defense responses to a virulent oomycete pathogen, through a process that is dependent on salicylic acid (SA) accumulation and activation of defense gene expression. Surprisingly, treatment with lower concentrations of cytokinin results in increased susceptibility. These functions for cytokinin in plant immunity require a host phosphorelay system and are mediated in part by type-A response regulators, which act as negative regulators of basal and pathogen-induced SA–dependent gene expression. Our results support a model in which cytokinin up-regulates plant immunity via an elevation of SA–dependent defense responses and in which SA in turn feedback-inhibits cytokinin signaling. The crosstalk between cytokinin and SA signaling networks may help plants fine-tune defense responses against pathogens

Multiple Myeloma Treatment in Real-world Clinical Practice : Results of a Prospective, Multinational, Noninterventional Study

Funding Information: The authors would like to thank all patients and their families and all the EMMOS investigators for their valuable contributions to the study. The authors would like to acknowledge Robert Olie for his significant contribution to the EMMOS study. Writing support during the development of our report was provided by Laura Mulcahy and Catherine Crookes of FireKite, an Ashfield company, a part of UDG Healthcare plc, which was funded by Millennium Pharmaceuticals, Inc, and Janssen Global Services, LLC. The EMMOS study was supported by research funding from Janssen Pharmaceutical NV and Millennium Pharmaceuticals, Inc. Funding Information: The authors would like to thank all patients and their families and all the EMMOS investigators for their valuable contributions to the study. The authors would like to acknowledge Robert Olie for his significant contribution to the EMMOS study. Writing support during the development of our report was provided by Laura Mulcahy and Catherine Crookes of FireKite, an Ashfield company, a part of UDG Healthcare plc, which was funded by Millennium Pharmaceuticals, Inc, and Janssen Global Services, LLC. The EMMOS study was supported by research funding from Janssen Pharmaceutical NV and Millennium Pharmaceuticals, Inc. Funding Information: M.M. has received personal fees from Janssen, Celgene, Amgen, Bristol-Myers Squibb, Sanofi, Novartis, and Takeda and grants from Janssen and Sanofi during the conduct of the study. E.T. has received grants from Janssen and personal fees from Janssen and Takeda during the conduct of the study, and grants from Amgen, Celgene/Genesis, personal fees from Amgen, Celgene/Genesis, Bristol-Myers Squibb, Novartis, and Glaxo-Smith Kline outside the submitted work. M.V.M. has received personal fees from Janssen, Celgene, Amgen, and Takeda outside the submitted work. M.C. reports honoraria from Janssen, outside the submitted work. M. B. reports grants from Janssen Cilag during the conduct of the study. M.D. has received honoraria for participation on advisory boards for Janssen, Celgene, Takeda, Amgen, and Novartis. H.S. has received honoraria from Janssen-Cilag, Celgene, Amgen, Bristol-Myers Squibb, Novartis, and Takeda outside the submitted work. V.P. reports personal fees from Janssen during the conduct of the study and grants, personal fees, and nonfinancial support from Amgen, grants and personal fees from Sanofi, and personal fees from Takeda outside the submitted work. W.W. has received personal fees and grants from Amgen, Celgene, Novartis, Roche, Takeda, Gilead, and Janssen and nonfinancial support from Roche outside the submitted work. J.S. reports grants and nonfinancial support from Janssen Pharmaceutical during the conduct of the study. V.L. reports funding from Janssen Global Services LLC during the conduct of the study and study support from Janssen-Cilag and Pharmion outside the submitted work. A.P. reports employment and shareholding of Janssen (Johnson & Johnson) during the conduct of the study. C.C. reports employment at Janssen-Cilag during the conduct of the study. C.F. reports employment at Janssen Research and Development during the conduct of the study. F.T.B. reports employment at Janssen-Cilag during the conduct of the study. The remaining authors have stated that they have no conflicts of interest. Publisher Copyright: © 2018 The AuthorsMultiple myeloma (MM) remains an incurable disease, with little information available on its management in real-world clinical practice. The results of the present prospective, noninterventional observational study revealed great diversity in the treatment regimens used to treat MM. Our results also provide data to inform health economic, pharmacoepidemiologic, and outcomes research, providing a framework for the design of protocols to improve the outcomes of patients with MM. Background: The present prospective, multinational, noninterventional study aimed to document and describe real-world treatment regimens and disease progression in multiple myeloma (MM) patients. Patients and Methods: Adult patients initiating any new MM therapy from October 2010 to October 2012 were eligible. A multistage patient/site recruitment model was applied to minimize the selection bias; enrollment was stratified by country, region, and practice type. The patient medical and disease features, treatment history, and remission status were recorded at baseline, and prospective data on treatment, efficacy, and safety were collected electronically every 3 months. Results: A total of 2358 patients were enrolled. Of these patients, 775 and 1583 did and did not undergo stem cell transplantation (SCT) at any time during treatment, respectively. Of the patients in the SCT and non-SCT groups, 49%, 21%, 14%, and 15% and 57%, 20%, 12% and 10% were enrolled at treatment line 1, 2, 3, and ≥ 4, respectively. In the SCT and non-SCT groups, 45% and 54% of the patients had received bortezomib-based therapy without thalidomide/lenalidomide, 12% and 18% had received thalidomide/lenalidomide-based therapy without bortezomib, and 30% and 4% had received bortezomib plus thalidomide/lenalidomide-based therapy as frontline treatment, respectively. The corresponding proportions of SCT and non-SCT patients in lines 2, 3, and ≥ 4 were 45% and 37%, 30% and 37%, and 12% and 3%, 33% and 27%, 35% and 32%, and 8% and 2%, and 27% and 27%, 27% and 23%, and 6% and 4%, respectively. In the SCT and non-SCT patients, the overall response rate was 86% to 97% and 64% to 85% in line 1, 74% to 78% and 59% to 68% in line 2, 55% to 83% and 48% to 60% in line 3, and 49% to 65% and 36% and 45% in line 4, respectively, for regimens that included bortezomib and/or thalidomide/lenalidomide. Conclusion: The results of our prospective study have revealed great diversity in the treatment regimens used to manage MM in real-life practice. This diversity was linked to factors such as novel agent accessibility and evolving treatment recommendations. Our results provide insight into associated clinical benefits.publishersversionPeer reviewe

An allele of Arabidopsis COI1 with hypo- and hypermorphic phenotypes in plant growth, defence and fertility

Resistance to biotrophic pathogens is largely dependent on the hormone salicylic acid (SA) while jasmonic acid (JA) regulates resistance against necrotrophs. JA negatively regulates SA and is, in itself, negatively regulated by SA. A key component of the JA signal transduction pathway is its receptor, the COI1 gene. Mutations in this gene can affect all the JA phenotypes, whereas mutations in other genes, either in JA signal transduction or in JA biosynthesis, lack this general effect. To identify components of the part of the resistance against biotrophs independent of SA, a mutagenised population of NahG plants (severely depleted of SA) was screened for suppression of susceptibility. The screen resulted in the identification of intragenic and extragenic suppressors, and the results presented here correspond to the characterization of one extragenic suppressor, coi1-40. coi1-40 is quite different from previously described coi1 alleles, and it represents a strategy for enhancing resistance to biotrophs with low levels of SA, likely suppressing NahG by increasing the perception to the remaining SA. The phenotypes of coi1-40 lead us to speculate about a modular function for COI1, since we have recovered a mutation in COI1 which has a number of JA-related phenotypes reduced while others are equal to or above wild type levels.This work was supported by grant BIO201018896 from "Ministerio de Economia y Competitividad" (MINECO) of Spain and by grant ACOMP/2012/105 from "Generalitat Valenciana" to PT, a JAE-CSIC Fellowship to JVC, a FPI-MINECO to AD, and Fellowships from the European Molecular Biology Organization and the Human Frontier Science Program to BBHW. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Dobón Alonso, A.; Wulff, BBH.; Canet Perez, JV.; Fort Rausell, P.; Tornero Feliciano, P. (2013). An allele of Arabidopsis COI1 with hypo- and hypermorphic phenotypes in plant growth, defence and fertility. PLoS ONE. 1(8):55115-55115. https://doi.org/10.1371/journal.pone.0055115S551155511518Vlot, A. C., Dempsey, D. A., & Klessig, D. F. (2009). Salicylic Acid, a Multifaceted Hormone to Combat Disease. Annual Review of Phytopathology, 47(1), 177-206. doi:10.1146/annurev.phyto.050908.135202Mauch, F., Mauch-Mani, B., Gaille, C., Kull, B., Haas, D., & Reimmann, C. (2001). Manipulation of salicylate content in Arabidopsis thaliana by the expression of an engineered bacterial salicylate synthase. The Plant Journal, 25(1), 67-77. doi:10.1046/j.1365-313x.2001.00940.xGaffney, T., Friedrich, L., Vernooij, B., Negrotto, D., Nye, G., Uknes, S., … Ryals, J. (1993). Requirement of Salicylic Acid for the Induction of Systemic Acquired Resistance. Science, 261(5122), 754-756. doi:10.1126/science.261.5122.754Delaney, T. P., Uknes, S., Vernooij, B., Friedrich, L., Weymann, K., Negrotto, D., … Ryals, J. (1994). A Central Role of Salicylic Acid in Plant Disease Resistance. Science, 266(5188), 1247-1250. doi:10.1126/science.266.5188.1247Lawton, K. (1995). Systemic Acquired Resistance inArabidopsisRequires Salicylic Acid but Not Ethylene. Molecular Plant-Microbe Interactions, 8(6), 863. doi:10.1094/mpmi-8-0863Ross, A. F. (1961). Systemic acquired resistance induced by localized virus infections in plants. Virology, 14(3), 340-358. doi:10.1016/0042-6822(61)90319-1Pieterse, C. M. ., & van Loon, L. C. (1999). Salicylic acid-independent plant defence pathways. Trends in Plant Science, 4(2), 52-58. doi:10.1016/s1360-1385(98)01364-8Fonseca, S., Chico, J. M., & Solano, R. (2009). The jasmonate pathway: the ligand, the receptor and the core signalling module. Current Opinion in Plant Biology, 12(5), 539-547. doi:10.1016/j.pbi.2009.07.013Ton, J., De Vos, M., Robben, C., Buchala, A., Métraux, J.-P., Van Loon, L. C., & Pieterse, C. M. J. (2002). Characterization ofArabidopsisenhanced disease susceptibility mutants that are affected in systemically induced resistance. The Plant Journal, 29(1), 11-21. doi:10.1046/j.1365-313x.2002.01190.xCui, J., Bahrami, A. K., Pringle, E. G., Hernandez-Guzman, G., Bender, C. L., Pierce, N. E., & Ausubel, F. M. (2005). Pseudomonas syringae manipulates systemic plant defenses against pathogens and herbivores. Proceedings of the National Academy of Sciences, 102(5), 1791-1796. doi:10.1073/pnas.0409450102Robert-Seilaniantz, A., Navarro, L., Bari, R., & Jones, J. D. (2007). Pathological hormone imbalances. Current Opinion in Plant Biology, 10(4), 372-379. doi:10.1016/j.pbi.2007.06.003Garcion, C., Lohmann, A., Lamodière, E., Catinot, J., Buchala, A., Doermann, P., & Métraux, J.-P. (2008). Characterization and Biological Function of the ISOCHORISMATE SYNTHASE2 Gene of Arabidopsis. Plant Physiology, 147(3), 1279-1287. doi:10.1104/pp.108.119420Tornero, P., Chao, R. A., Luthin, W. N., Goff, S. A., & Dangl, J. L. (2002). Large-Scale Structure –Function Analysis of the Arabidopsis RPM1 Disease Resistance Protein. The Plant Cell, 14(2), 435-450. doi:10.1105/tpc.010393Bowling, S. A., Guo, A., Cao, H., Gordon, A. S., Klessig, D. F., & Dong, X. (1994). A mutation in Arabidopsis that leads to constitutive expression of systemic acquired resistance. The Plant Cell, 6(12), 1845-1857. doi:10.1105/tpc.6.12.1845Bowling, S. A., Clarke, J. D., Liu, Y., Klessig, D. F., & Dong, X. (1997). The cpr5 mutant of Arabidopsis expresses both NPR1-dependent and NPR1-independent resistance. The Plant Cell, 9(9), 1573-1584. doi:10.1105/tpc.9.9.1573Yu, I. -c., Parker, J., & Bent, A. F. (1998). Gene-for-gene disease resistance without the hypersensitive response in Arabidopsis dnd1 mutant. Proceedings of the National Academy of Sciences, 95(13), 7819-7824. doi:10.1073/pnas.95.13.7819Dietrich, R. A., Delaney, T. P., Uknes, S. J., Ward, E. R., Ryals, J. A., & Dangl, J. L. (1994). Arabidopsis mutants simulating disease resistance response. Cell, 77(4), 565-577. doi:10.1016/0092-8674(94)90218-6Rivas-San Vicente, M., & Plasencia, J. (2011). Salicylic acid beyond defence: its role in plant growth and development. Journal of Experimental Botany, 62(10), 3321-3338. doi:10.1093/jxb/err031Wang, D. (2005). Induction of Protein Secretory Pathway Is Required for Systemic Acquired Resistance. Science, 308(5724), 1036-1040. doi:10.1126/science.1108791Ritter, C. (1995). TheavrRpm1Gene ofPseudomonas syringaepv.maculicolaIs Required for Virulence on Arabidopsis. Molecular Plant-Microbe Interactions, 8(3), 444. doi:10.1094/mpmi-8-0444Debener, T., Lehnackers, H., Arnold, M., & Dangl, J. L. (1991). Identification and molecular mapping of a single Arabidopsis thaliana locus determining resistance to a phytopathogenic Pseudomonas syringae isolate. The Plant Journal, 1(3), 289-302. doi:10.1046/j.1365-313x.1991.t01-7-00999.xGrant, M., Godiard, L., Straube, E., Ashfield, T., Lewald, J., Sattler, A., … Dangl, J. (1995). Structure of the Arabidopsis RPM1 gene enabling dual specificity disease resistance. Science, 269(5225), 843-846. doi:10.1126/science.7638602Mindrinos, M., Katagiri, F., Yu, G.-L., & Ausubel, F. M. (1994). The A. thaliana disease resistance gene RPS2 encodes a protein containing a nucleotide-binding site and leucine-rich repeats. Cell, 78(6), 1089-1099. doi:10.1016/0092-8674(94)90282-8Coego, A., Ramirez, V., Gil, M. J., Flors, V., Mauch-Mani, B., & Vera, P. (2005). An Arabidopsis Homeodomain Transcription Factor, OVEREXPRESSOR OF CATIONIC PEROXIDASE 3, Mediates Resistance to Infection by Necrotrophic Pathogens. The Plant Cell, 17(7), 2123-2137. doi:10.1105/tpc.105.032375Pieterse, C. M. J., van Wees, S. C. M., van Pelt, J. A., Knoester, M., Laan, R., Gerrits, H., … van Loon, L. C. (1998). A Novel Signaling Pathway Controlling Induced Systemic Resistance in Arabidopsis. The Plant Cell, 10(9), 1571-1580. doi:10.1105/tpc.10.9.1571Berger, S., Bell, E., & Mullet, J. E. (1996). Two Methyl Jasmonate-Insensitive Mutants Show Altered Expression of AtVsp in Response to Methyl Jasmonate and Wounding. Plant Physiology, 111(2), 525-531. doi:10.1104/pp.111.2.525Attaran, E., Zeier, T. E., Griebel, T., & Zeier, J. (2009). Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance in Arabidopsis. The Plant Cell, 21(3), 954-971. doi:10.1105/tpc.108.063164Yan, J., Zhang, C., Gu, M., Bai, Z., Zhang, W., Qi, T., … Xie, D. (2009). The Arabidopsis CORONATINE INSENSITIVE1 Protein Is a Jasmonate Receptor. The Plant Cell, 21(8), 2220-2236. doi:10.1105/tpc.109.065730Mittal, S. (1995). Role of the Phytotoxin Coronatine in the Infection ofAmbidopsis thalianabyPseudomonas syringaepv.tomato. Molecular Plant-Microbe Interactions, 8(1), 165. doi:10.1094/mpmi-8-0165Genoud, T., & Métraux, J.-P. (1999). Crosstalk in plant cell signaling: structure and function of the genetic network. Trends in Plant Science, 4(12), 503-507. doi:10.1016/s1360-1385(99)01498-3Lawton, K. A., Friedrich, L., Hunt, M., Weymann, K., Delaney, T., Kessmann, H., … Ryals, J. (1996). Benzothiadiazole induces disease resistance in Arabidopsis by activation of the systemic acquired resistance signal transduction pathway. The Plant Journal, 10(1), 71-82. doi:10.1046/j.1365-313x.1996.10010071.xFeys, B., Benedetti, C. E., Penfold, C. N., & Turner, J. G. (1994). Arabidopsis Mutants Selected for Resistance to the Phytotoxin Coronatine Are Male Sterile, Insensitive to Methyl Jasmonate, and Resistant to a Bacterial Pathogen. The Plant Cell, 751-759. doi:10.1105/tpc.6.5.751Sun, J., Xu, Y., Ye, S., Jiang, H., Chen, Q., Liu, F., … Li, C. (2009). Arabidopsis ASA1 Is Important for Jasmonate-Mediated Regulation of Auxin Biosynthesis and Transport during Lateral Root Formation. The Plant Cell, 21(5), 1495-1511. doi:10.1105/tpc.108.064303He, Y., Fukushige, H., Hildebrand, D. F., & Gan, S. (2002). Evidence Supporting a Role of Jasmonic Acid in Arabidopsis Leaf Senescence. Plant Physiology, 128(3), 876-884. doi:10.1104/pp.010843Shan, X., Zhang, Y., Peng, W., Wang, Z., & Xie, D. (2009). Molecular mechanism for jasmonate-induction of anthocyanin accumulation in Arabidopsis. Journal of Experimental Botany, 60(13), 3849-3860. doi:10.1093/jxb/erp223Yoshida, Y., Sano, R., Wada, T., Takabayashi, J., & Okada, K. (2009). Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning in Arabidopsis. Development, 136(6), 1039-1048. doi:10.1242/dev.030585Borevitz, J. O., Xia, Y., Blount, J., Dixon, R. A., & Lamb, C. (2000). Activation Tagging Identifies a Conserved MYB Regulator of Phenylpropanoid Biosynthesis. The Plant Cell, 12(12), 2383-2393. doi:10.1105/tpc.12.12.2383Berger, S., Bell, E., Sadka, A., & Mullet, J. E. (1995). Arabidopsis thaliana Atvsp is homologous to soybean VspA and VspB, genes encoding vegetative storage protein acid phosphatases, and is regulated similarly by methyl jasmonate, wounding, sugars, light and phosphate. Plant Molecular Biology, 27(5), 933-942. doi:10.1007/bf00037021Feng, S., Ma, L., Wang, X., Xie, D., Dinesh-Kumar, S. P., Wei, N., & Deng, X. W. (2003). The COP9 Signalosome Interacts Physically with SCFCOI1 and Modulates Jasmonate Responses. The Plant Cell, 15(5), 1083-1094. doi:10.1105/tpc.010207Nawrath C, Métraux JP, Genoud T (2005) Chemical signals in plant resistance: salicylic acid. . In: Tuzun S, Bent E, editors. Multigenic and Induced Systemic Resistance in Plants. Dordrecht, Netherlands.: Springer US. pp. pp. 143–165.Kunkel, B. N., & Brooks, D. M. (2002). Cross talk between signaling pathways in pathogen defense. Current Opinion in Plant Biology, 5(4), 325-331. doi:10.1016/s1369-5266(02)00275-3Truman, W., Bennett, M. H., Kubigsteltig, I., Turnbull, C., & Grant, M. (2007). Arabidopsissystemic immunity uses conserved defense signaling pathways and is mediated by jasmonates. Proceedings of the National Academy of Sciences, 104(3), 1075-1080. doi:10.1073/pnas.0605423104Canet, J. V., Dobón, A., Ibáñez, F., Perales, L., & Tornero, P. (2010). Resistance and biomass in Arabidopsis: a new model for Salicylic Acid perception. Plant Biotechnology Journal, 8(2), 126-141. doi:10.1111/j.1467-7652.2009.00468.xCasimiro, I., Marchant, A., Bhalerao, R. P., Beeckman, T., Dhooge, S., Swarup, R., … Bennett, M. (2001). Auxin Transport Promotes Arabidopsis Lateral Root Initiation. The Plant Cell, 13(4), 843-852. doi:10.1105/tpc.13.4.843Celenza, J. L., Grisafi, P. L., & Fink, G. R. (1995). A pathway for lateral root formation in Arabidopsis thaliana. Genes & Development, 9(17), 2131-2142. doi:10.1101/gad.9.17.2131Traw, M. B., & Bergelson, J. (2003). Interactive Effects of Jasmonic Acid, Salicylic Acid, and Gibberellin on Induction of Trichomes in Arabidopsis. Plant Physiology, 133(3), 1367-1375. doi:10.1104/pp.103.027086Kloek, A. P., Verbsky, M. L., Sharma, S. B., Schoelz, J. E., Vogel, J., Klessig, D. F., & Kunkel, B. N. (2001). Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine-insensitive (coi1) mutation occurs through two distinct mechanisms. The Plant Journal, 26(5), 509-522. doi:10.1046/j.1365-313x.2001.01050.xXie, D. (1998). COI1: An Arabidopsis Gene Required for Jasmonate-Regulated Defense and Fertility. Science, 280(5366), 1091-1094. doi:10.1126/science.280.5366.1091Ellis, C., & Turner, J. (2002). A conditionally fertile coi1 allele indicates cross-talk between plant hormone signalling pathways in Arabidopsis thaliana seeds and young seedlings. Planta, 215(4), 549-556. doi:10.1007/s00425-002-0787-4Fernández-Arbaizar, A., Regalado, J. J., & Lorenzo, O. (2011). Isolation and Characterization of Novel Mutant Loci Suppressing the ABA Hypersensitivity of the Arabidopsis coronatine insensitive 1-16 (coi1-16) Mutant During Germination and Seedling Growth. Plant and Cell Physiology, 53(1), 53-63. doi:10.1093/pcp/pcr174He, Y., Chung, E.-H., Hubert, D. A., Tornero, P., & Dangl, J. L. (2012). Specific Missense Alleles of the Arabidopsis Jasmonic Acid Co-Receptor COI1 Regulate Innate Immune Receptor Accumulation and Function. PLoS Genetics, 8(10), e1003018. doi:10.1371/journal.pgen.1003018Xu, L., Liu, F., Lechner, E., Genschik, P., Crosby, W. L., Ma, H., … Xie, D. (2002). The SCFCOI1 Ubiquitin-Ligase Complexes Are Required for Jasmonate Response in Arabidopsis. The Plant Cell, 14(8), 1919-1935. doi:10.1105/tpc.003368Chini, A., Fonseca, S., Fernández, G., Adie, B., Chico, J. M., Lorenzo, O., … Solano, R. (2007). The JAZ family of repressors is the missing link in jasmonate signalling. Nature, 448(7154), 666-671. doi:10.1038/nature06006Grunewald, W., Vanholme, B., Pauwels, L., Plovie, E., Inzé, D., Gheysen, G., & Goossens, A. (2009). Expression of the Arabidopsis jasmonate signalling repressor JAZ1/TIFY10A is stimulated by auxin. EMBO reports, 10(8), 923-928. doi:10.1038/embor.2009.103Cao, H., Glazebrook, J., Clarke, J. D., Volko, S., & Dong, X. (1997). The Arabidopsis NPR1 Gene That Controls Systemic Acquired Resistance Encodes a Novel Protein Containing Ankyrin Repeats. Cell, 88(1), 57-63. doi:10.1016/s0092-8674(00)81858-9Century, K. S., Holub, E. B., & Staskawicz, B. J. (1995). NDR1, a locus of Arabidopsis thaliana that is required for disease resistance to both a bacterial and a fungal pathogen. Proceedings of the National Academy of Sciences, 92(14), 6597-6601. doi:10.1073/pnas.92.14.6597Wildermuth, M. C., Dewdney, J., Wu, G., & Ausubel, F. M. (2001). Isochorismate synthase is required to synthesize salicylic acid for plant defence. Nature, 414(6863), 562-565. doi:10.1038/35107108Lu, M., Tang, X., & Zhou, J.-M. (2001). Arabidopsis NHO1 Is Required for General Resistance against Pseudomonas Bacteria. The Plant Cell, 13(2), 437-447. doi:10.1105/tpc.13.2.437Ritter, C., & Dangl, J. L. (1996). Interference between Two Specific Pathogen Recognition Events Mediated by Distinct Plant Disease Resistance Genes. The Plant Cell, 251-257. doi:10.1105/tpc.8.2.251Tornero, P., & Dangl, J. L. (2002). A high-throughput method for quantifying growth of phytopathogenic bacteria in Arabidopsis thaliana. The Plant Journal, 28(4), 475-481. doi:10.1046/j.1365-313x.2001.01136.xMacho, A. P., Guevara, C. M., Tornero, P., Ruiz-Albert, J., & Beuzón, C. R. (2010). The Pseudomonas syringae effector protein HopZ1a suppresses effector-triggered immunity. New Phytologist, 187(4), 1018-1033. doi:10.1111/j.1469-8137.2010.03381.xTon, J., & Mauch-Mani, B. (2004). β-amino-butyric acid-induced resistance against necrotrophic pathogens is based on ABA-dependent priming for callose. The Plant Journal, 38(1), 119-130. doi:10.1111/j.1365-313x.2004.02028.xCANET, J. V., DOBÓN, A., ROIG, A., & TORNERO, P. (2010). Structure-function analysis of npr1 alleles in Arabidopsis reveals a role for its paralogs in the perception of salicylic acid. Plant, Cell & Environment, 33(11), 1911-1922. doi:10.1111/j.1365-3040.2010.02194.xJohnson, C. M., Stout, P. R., Broyer, T. C., & Carlton, A. B. (1957). Comparative chlorine requirements of different plant species. Plant and Soil, 8(4), 337-353. doi:10.1007/bf01666323Dobón, A., Canet, J. V., Perales, L., & Tornero, P. (2011). Quantitative genetic analysis of salicylic acid perception in Arabidopsis. Planta, 234(4), 671-684. doi:10.1007/s00425-011-1436-6Mehrtens, F., Kranz, H., Bednarek, P., & Weisshaar, B. (2005). The Arabidopsis Transcription Factor MYB12 Is a Flavonol-Specific Regulator of Phenylpropanoid Biosynthesis. Plant Physiology, 138(2), 1083-1096. doi:10.1104/pp.104.058032Konieczny, A., & Ausubel, F. M. (1993). A procedure for mapping Arabidopsis mutations using co-dominant ecotype-specific PCR-based markers. The Plant Journal, 4(2), 403-410. doi:10.1046/j.1365-313x.1993.04020403.xBell, C. J., & Ecker, J. R. (1994). Assignment of 30 Microsatellite Loci to the Linkage Map of Arabidopsis. Genomics, 19(1), 137-144. doi:10.1006/geno.1994.1023Swarbreck, D., Wilks, C., Lamesch, P., Berardini, T. Z., Garcia-Hernandez, M., Foerster, H., … Huala, E. (2007). The Arabidopsis Information Resource (TAIR): gene structure and function annotation. Nucleic Acids Research, 36(Database), D1009-D1014. doi:10.1093/nar/gkm965Jürgens G, Mayer U, Torres Ruiz RA, Berleth T, Mísera S (1991) Genetic analysis of pattern formation in the Arabidopsis embryo. Development (Supplement 1) : 27–38.Huang, W. E., Wang, H., Zheng, H., Huang, L., Singer, A. C., Thompson, I., & Whiteley, A. S. (2005). Chromosomally located gene fusions constructed in Acinetobacter sp. ADP1 for the detection of salicylate. Environmental Microbiology, 7(9), 1339-1348. doi:10.1111/j.1462-5822.2005.00821.xDeFraia, C. T., Schmelz, E. A., & Mou, Z. (2008). A rapid biosensor-based method for quantification of free and glucose-conjugated salicylic acid. Plant Methods, 4(1), 28. doi:10.1186/1746-4811-4-28Chenna, R. (2003). Multiple sequence alignment with the Clustal series of programs. Nucleic Acids Research, 31(13), 3497-3500. doi:10.1093/nar/gkg50

H. B. Smith, Non-aristotelian Logic - Letters on Logic to a young man without a master - Foundations of formal Logic

Feys Robert. H. B. Smith, Non-aristotelian Logic - Letters on Logic to a young man without a master - Foundations of formal Logic. In: Revue néo-scolastique de philosophie. 26ᵉ année, Deuxième série, n°4, 1924. pp. 486-488

André Darbon, Les catégories de la modalité. Publié par Madeleine Lagarce-Darbon

Feys Robert. André Darbon, Les catégories de la modalité. Publié par Madeleine Lagarce-Darbon. In: Revue Philosophique de Louvain. Troisième série, tome 55, n°45, 1957. p. 123

Les logiques nouvelles des modalités (suite et fin)

Feys Robert. Les logiques nouvelles des modalités (suite et fin). In: Revue néo-scolastique de philosophie. 41ᵉ année, Deuxième série, n°58, 1938. pp. 217-252