scholarly journals Maize 9-Lipoxygenase ZmLOX3 Controls Development, Root-Specific Expression of Defense Genes, and Resistance to Root-Knot Nematodes

2008 ◽  
Vol 21 (1) ◽  
pp. 98-109 ◽  
Author(s):  
Xiquan Gao ◽  
James Starr ◽  
Cornelia Göbel ◽  
Jürgen Engelberth ◽  
Ivo Feussner ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Meloidogyne Incognita ◽  
Phenylalanine Ammonia Lyase ◽  
Nematode Resistance ◽  
Normal Plant ◽  
Wild Type ◽  
Specific Expression ◽  
Root Knot Nematodes ◽  
Knockout Mutants ◽  
Plant Nematode

Root-knot nematodes (RKN) are severe pests of maize. Although lipoxygenase (LOX) pathways and their oxylipin products have been implicated in plant–nematode interactions, prior to this report there was no conclusive genetic evidence for the function of any plant LOX gene in such interactions. We showed that expression of a maize 9-LOX gene, ZmLOX3, increased steadily and peaked at 7 days after inoculation with Meloidogyne incognita RKN. Mu-insertional lox3-4 mutants displayed increased attractiveness to RKN and an increased number of juveniles and eggs. A set of jasmonic acid (JA)- and ethylene (ET)-responsive and biosynthetic genes as well as salicylic acid (SA)-dependent genes were overexpressed specifically in the roots of lox3-4 mutants. Consistent with this, levels of JA, SA, and ET were elevated in lox3-4 mutant roots, but not in leaves. Unlike wild types, in lox3-4 mutant roots, a phenylalanine ammonia lyase (PAL) gene was not RKN-inducible, suggesting a role for PAL-mediated metabolism in nematode resistance. In addition to these alterations in the defense status of roots, lox3-4 knockout mutants displayed precocious senescence and reduced root length and plant height compared with the wild type, suggesting that ZmLOX3 is required for normal plant development. Taken together, our data indicate that the ZmLOX3-mediated pathway may act as a root-specific suppressor of all three major defense signaling pathways to channel plant energy into growth processes, but is required for normal levels of resistance against nematodes.

scholarly journals ­­­grapevine (Vitis Spp.) Rootstock Stilbenoid Associations With Host Resistance to and Induction by Root Knot Nematodes, Meloidogyne Incognita

2020 ◽  
Author(s):  
Christopher Wallis
Keyword(s):  
Meloidogyne Incognita ◽  
Host Resistance ◽  
Nematode Resistance ◽  
Cabernet Sauvignon ◽  
Healthy Controls ◽  
Mechanisms Of Resistance ◽  
Breeding Programs ◽  
Root Knot Nematodes ◽  
Vitis Spp ◽  
Over Time

Abstract Objective:The root knot nematodes (RKN)Meloidogyne incognita can severely reduce grapevine yields over time. Grapevine rootstocks have been developed from wild Vitis species that provide resistance to nematode infections. However, the potential biochemical or mechanical mechanisms of resistance have not been thoroughly explored. Therefore, this study measured levels of stilbenoids in roots of non-infected and RKN-infected grapevines with Cabernet Sauvignon scion grafted to susceptible (O39-16) or resistant (Freedom) rootstocks. This was part of a larger effort to assess phenolic compound levels within grapevine rootstocks to determine roles of stilbenoidcompounds in improving nematode resistance and overall plant health.Results: None of the assessed compounds were consistently greater in RKN infected plants versus healthy controls. Stilbenoids putatively identified as pallidol, ɑ-viniferin, miyabenol C, and hopeaphenol were overall much greater in Freedom than O39-16 rootstocks. By contrast, the stilbenoids ampelopsin A, ω-viniferin, and vitisin B were greater in O39-16 than Freedom. O39-16 and Freedom had similar levels of other stilbenoids especially monomers and dimers. Potentially the greater levels of specific stilbenoids present in Freedom than O39-16 provided RKN resistance. If validated, breeding programs could utilize the increased presence of these compounds as a marker for increased resistance to nematodes.

Salicylic acid-induced suppression of Meloidogyne incognita infestation of okra and cowpea

Nematology ◽  
2003 ◽  
Vol 5 (5) ◽  
pp. 747-752 ◽  
Author(s):  
Bidyut Nandi ◽  
Santi Prasad Sinha Babu ◽  
Nirmalya Banerjee ◽  
Kabita Kundu
Keyword(s):  
Salicylic Acid ◽  
Meloidogyne Incognita ◽  
Phenylalanine Ammonia Lyase ◽  
Foliar Spray ◽  
In Vitro Test ◽  
Pal Activity ◽  
Pathogenesis Related Protein ◽  
Pathogenesis Related ◽  
Vitro Test

AbstractSalicylic acid (SA) applied as 10 mM foliar spray to okra (Abelmoschus esculentus) cv. Purbani Kranti and cowpea (Vigna unguiculata) cv. Pusa Ruby plants 24 h before inoculation of roots with Meloidogyne incognita juveniles, reduced infestation. Salicylic acid had no direct influence on plant growth and did not kill nematodes in an in vitro test. It induced increased accumulation of a 14 kDa pathogenesis-related protein (PR-1) in roots of both non-inoculated and inoculated salicylic acid-sprayed okra but not in the treated leaves. Salicylic acid sprays enhanced phenylalanine ammonia lyase (PAL) activity in roots of both non-inoculated and inoculated cowpea, estimated at 15 days after inoculation. Infected roots had higher PAL activity than roots of the corresponding non-inoculated treatments. Both PAL activity and SA-induced resistance gradually declined with plant age after treatment.

Hairy roots to test for transgenic nematode resistance: think twice

Nematology ◽  
2003 ◽  
Vol 5 (6) ◽  
pp. 831-841 ◽  
Author(s):  
Eva Plovie ◽  
Sylvie De Buck ◽  
Els Goeleven ◽  
Miek Tanghe ◽  
Isabel Vercauteren ◽  
...  
Keyword(s):  
Hairy Roots ◽  
Meloidogyne Incognita ◽  
Nematode Resistance ◽  
Control Group ◽  
Wild Type ◽  
Feeding Sites ◽  
Second Stage ◽  
Antisense Orientation ◽  
Transgenic Hairy Roots ◽  
Transgenic Lines

Abstract Hairy roots induced by Agrobacterium rhizogenes have been proposed as a versatile, easy and reproducible system for testing nematode resistance in crop plants. Here, A. rhizogenes was used to induce transgenic hairy roots on tomato (Lycopersicon esculentum) containing the LEMMI9 cDNA in sense and/or antisense orientation under control of a nematode responsive promoter. The purpose was to inhibit the expression of this gene that is strongly activated in the nematode-induced feeding sites in order to block their development and, thus, make the plants resistant. Several LEMMI9 transgenic lines produced fewer Meloidogyne incognita second-stage juveniles than the control lines, but a large variation in progeny was also seen among the control lines. Therefore, we recommend that several independent wild-type hairy root lines are generated and tested to obtain a solid control group for evaluating putative resistance constructs.

The involvement of phenylalanine ammonia-lyase and salicylic acid in the induction of resistance of tomato plants infested with gall nematode Meloidogyne incognita

2007 ◽  
Vol 416 (1) ◽  
pp. 382-385 ◽  
Author(s):  
N. I. Vasyukova ◽  
S. M. Pridvorova ◽  
N. G. Gerasimova ◽  
G. I. Chalenko ◽  
O. L. Ozeretskovskaya ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Meloidogyne Incognita ◽  
Phenylalanine Ammonia Lyase ◽  
Tomato Plants ◽  
Induction Of Resistance

scholarly journals Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Abiotic Stress ◽  
Wild Type ◽  
Pr Genes ◽  
Genes Expression ◽  
Salicylic Acid Accumulation ◽  
Cell Death Phenotype ◽  
Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

scholarly journals The contribution of PIP2-type aquaporins to photosynthetic response to increased vapour pressure deficit

2021 ◽  
Author(s):  
D Israel ◽  
S Khan ◽  
C R Warren ◽  
J J Zwiazek ◽  
T M Robson
Keyword(s):  
Vapour Pressure Deficit ◽  
Air Humidity ◽  
Wild Type ◽  
Knockout Mutant ◽  
Evaporative Demand ◽  
Co2 Transport ◽  
Whole Plant ◽  
Knockout Mutants ◽  
Leaf Level ◽  
Low Humidity

Abstract The roles of different plasma membrane aquaporins (PIPs) in leaf-level gas exchange of Arabidopsis thaliana were examined using knockout mutants. Since multiple Arabidopsis PIPs are implicated in CO2 transport across cell membranes, we focused on identifying the effects of the knockout mutations on photosynthesis, and whether they are mediated through the control of stomatal conductance of water vapour (gs), mesophyll conductance of CO2 (gm) or both. We grew Arabidopsis plants in low and high humidity environments and found that the contribution of PIPs to gs was larger under low air humidity when the evaporative demand was high, whereas any effect of lacking PIP function was minimal under higher humidity. The pip2;4 knockout mutant had 44% higher gs than the wild type plants under low humidity, which in turn resulted in an increased net photosynthetic rate (Anet). We also observed a 23% increase in whole-plant transpiration (E) for this knockout mutant. The lack of functional AtPIP2;5 did not affect gs or E, but resulted in homeostasis of gm despite changes of humidity, indicating a possible role in regulating CO2 membrane permeability. CO2 transport measurements in yeast expressing AtPIP2;5 confirmed that this aquaporin is indeed permeable to CO2.

scholarly journals Uncoupling Salicylic Acid-Dependent Cell Death and Defense-Related Responses From Disease Resistance in the Arabidopsis Mutant acd5

Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 341-350
Author(s):  
Jean T Greenberg ◽  
F Paul Silverman ◽  
Hua Liang
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Higher Plants ◽  
Ethylene Signaling ◽  
Symptom Development ◽  
Wild Type ◽  
Dependent Cell ◽  
Arabidopsis Mutant

Abstract Salicylic acid (SA) is required for resistance to many diseases in higher plants. SA-dependent cell death and defense-related responses have been correlated with disease resistance. The accelerated cell death 5 mutant of Arabidopsis provides additional genetic evidence that SA regulates cell death and defense-related responses. However, in acd5, these events are uncoupled from disease resistance. acd5 plants are more susceptible to Pseudomonas syringae early in development and show spontaneous SA accumulation, cell death, and defense-related markers later in development. In acd5 plants, cell death and defense-related responses are SA dependent but they do not confer disease resistance. Double mutants with acd5 and nonexpressor of PR1, in which SA signaling is partially blocked, show greatly attenuated cell death, indicating a role for NPR1 in controlling cell death. The hormone ethylene potentiates the effects of SA and is important for disease symptom development in Arabidopsis. Double mutants of acd5 and ethylene insensitive 2, in which ethylene signaling is blocked, show decreased cell death, supporting a role for ethylene in cell death control. We propose that acd5 plants mimic P. syringae-infected wild-type plants and that both SA and ethylene are normally involved in regulating cell death during some susceptible pathogen infections.

scholarly journals Transcriptome Analysis of Eggplant Root in Response to Root-Knot Nematode Infection

Pathogens ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 470
Author(s):  
Min Zhang ◽  
Hongyuan Zhang ◽  
Jie Tan ◽  
Shuping Huang ◽  
Xia Chen ◽  
...  
Keyword(s):  
Defense Mechanisms ◽  
Expression Profiles ◽  
Resistance Mechanism ◽  
Solanum Melongena ◽  
Enrichment Analysis ◽  
Nematode Resistance ◽  
Differentially Expressed ◽  
Root Knot Nematode ◽  
Solanum Torvum ◽  
Plant Nematode

Eggplant (Solanum melongena L.), which belongs to the Solanaceae family, is an important vegetable crop. However, its production is severely threatened by root-knot nematodes (RKNs) in many countries. Solanum torvum, a wild relative of eggplant, is employed worldwide as rootstock for eggplant cultivation due to its resistance to soil-borne diseases such as RKNs. In this study, to identify the RKN defense mechanisms, the transcriptomic profiles of eggplant and Solanum torvum were compared. A total of 5360 differentially expressed genes (DEGs) were identified for the response to RKN infection. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that these DEGs are mainly involved in the processes of response to stimulus, protein phosphorylation, hormone signal transduction, and plant-pathogen interaction pathways. Many phytohormone-related genes and transcription factors (MYB, WRKY, and NAC) were differentially expressed at the four time points (ck, 7, 14, and 28 days post-infection). The abscisic acid signaling pathway might be involved in plant-nematode interactions. qRT-PCR validated the expression levels of some of the DEGs in eggplant. These findings demonstrate the nematode-induced expression profiles and provide some insights into the nematode resistance mechanism in eggplant.

Abnormal Spinal Cord Myelination due to Oligodendrocyte Dysfunction in a Model of Huntington’s Disease

2021 ◽  
pp. 1-8
Author(s):  
Costanza Ferrari Bardile ◽  
Harwin Sidik ◽  
Reynard Quek ◽  
Nur Amirah Binte Mohammad Yusof ◽  
Marta Garcia-Miralles ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Oligodendrocyte Progenitor Cells ◽  
Wild Type ◽  
Specific Expression ◽  
Relative Contribution ◽  
Related Proteins ◽  
The Impact ◽  
Cervical Area

Background: The relative contribution of grey matter (GM) and white matter (WM) degeneration to the progressive brain atrophy in Huntington’s disease (HD) has been well studied. The pathology of the spinal cord in HD is comparatively less well documented. Objective: We aim to characterize spinal cord WM abnormalities in a mouse model of HD and evaluate whether selective removal of mutant huntingtin (mHTT) from oligodendroglia rescues these deficits. Methods: Histological assessments were used to determine the area of GM and WM in the spinal cord of 12-month-old BACHD mice, while electron microscopy was used to analyze myelin fibers in the cervical area of the spinal cord. To investigate the impact of inactivation of mHTT in oligodendroglia on these measures, we used the previously described BACHDxNG2Cre mouse line where mHTT is specifically reduced in oligodendrocyte progenitor cells. Results: We show that spinal GM and WM areas are significantly atrophied in HD mice compared to wild-type controls. We further demonstrate that specific reduction of mHTT in oligodendroglial cells rescues the atrophy of spinal cord WM, but not GM, observed in HD mice. Inactivation of mHTT in oligodendroglia had no effect on the density of oligodendroglial cells but enhanced the expression of myelin-related proteins in the spinal cord. Conclusion: Our findings demonstrate that the myelination abnormalities observed in brain WM structures in HD extend to the spinal cord and suggest that specific expression of mHTT in oligodendrocytes contributes to such abnormalities.

scholarly journals Tissue-specific expression of B7x protects from CD4 T cell–mediated autoimmunity

2011 ◽  
Vol 208 (8) ◽  
pp. 1683-1694 ◽  
Author(s):  
Joyce Wei ◽  
P’ng Loke ◽  
Xingxing Zang ◽  
James P. Allison
Keyword(s):  
T Cells ◽  
Pancreatic Islets ◽  
Peripheral Tolerance ◽  
Wild Type ◽  
Autoimmune Encephalomyelitis ◽  
Specific Expression ◽  
Tissue Specific ◽  
Disease Induction ◽  
Deficient Mice ◽  
Experimental Autoimmune

B7x, an inhibitory member of the B7/CD28 superfamily, is highly expressed in a broad range of nonhematopoietic organs, suggesting a role in maintaining peripheral tolerance. As endogenous B7x protein is expressed in pancreatic islets, we investigated whether the molecule inhibits diabetogenic responses. Transfer of disease-inducing BDC2.5 T cells into B7x-deficient mice resulted in a more aggressive form of diabetes than in wild-type animals. This exacerbation of disease correlated with higher frequencies of islet-infiltrating Th1 and Th17 cells. Conversely, local B7x overexpression inhibited the development of autoimmunity, as crossing diabetes-susceptible BDC2.5/B6g7 mice to animals overexpressing B7x in pancreatic islets abrogated disease induction. This protection was caused by the inhibition of IFN-γ production by CD4 T cells and not to a skewing or expansion of Th2 or regulatory T cells. The suppressive function of B7x was also supported by observations from another autoimmune model, experimental autoimmune encephalomyelitis, in which B7x-deficient mice developed exacerbated disease in comparison with wild-type animals. Analysis of central nervous system–infiltrating immune cells revealed that the loss of endogenous B7x resulted in expanded Th1 and Th17 responses. Data from these two autoimmune models provide evidence that B7x expression in the periphery acts as an immune checkpoint to prevent tissue-specific autoimmunity.

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