Lesion growth and virus localization in leaves of Nicotiana tabacum cv. Xanthi nc. after inoculation with tobacco mosaic virus and incubation alternately at 22°C and 32°C

Weststeijn, Emma A.

doi:10.1016/s0048-4059(81)80086-0

Cited by 56 publications

(33 citation statements)

References 12 publications

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“…The corresponding Avr ligand has been identified as the viral replicase (Padgett and Beachy, 1993). At 2OoC, N-mediated resistance is functional, but it is inactive at 3OoC (Weststeijn, 1981). The temperature sensitivity of this interaction provides a molecular switch to study the activation of N gene-dependent defense responses in leaves.…”

Section: Tobacco N Gene-mediated Resistance To Tmvmentioning

confidence: 99%

Resistance gene-dependent plant defense responses.

1996

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Section: Tobacco N Gene-mediated Resistance To Tmvmentioning

confidence: 99%

Resistance gene-dependent plant defense responses.

1996

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“…The rapid and precisely timed development of PR-1 gene induction and necrosis after the temperature shift allowed us to demonstrate that SA increases preceded the induction of the PR-1 genes by at least 2 hr and the appearance of necrotic lesions by 3 to 5 hr. Interestingly, Weststeijn (1981) showed that when tobacco plants infected at 32OC were transferred to 22OC for short periods of time and then returned to the elevated temperature, ' Label remaining in aqueous phase after extraction of free and P-glucosidase-released SA.…”

Section: Analysis Of the Fate Of Exogenously Supplied Samentioning

confidence: 99%

Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection.

1992

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lncreases in endogenous salicylic acid (SA) levels and induction of several families of pathogenesis-related genes (PR-1 through PR-5) occur during the resistance response of tobacco to tobacco mosaic virus infection. We found that at temperatures that prevent the induction of PR genes and resistance, the increases in SA levels were eliminated. The addition of exogenous SA to infected plants at these temperatures was sufficient to induce the PR genes but not the hypersensitive response. However, when the resistance response was restored by shifting infected plants to permissive temperatures, SA levels increased dramatically and preceded PR-1 gene expression and necrotic lesion formation associated with resistance. SA was also found in a conjugated form whose levels increased in parallel with the free SA levels. The majority of the conjugates appeared to be SA glucosides. The same glucoside was formed when plants were supplied with exogenous SA. These results provide further evidence that endogenous SA signals the induction of certain defense responses and suggests additional complexity in the modulation of this signal.

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“…Perturbation of Avr or R genes (15,20,41), graft inoculation instead of mechanical inoculation (6,28,69,72), change in genetic background of the R gene-carrying plant (45), heterozygosity rather than homozygosity of the R-genotype plant (10,52,56), prevention of salicylic acid accumulation in the R-genotype plant (19,42), or temperature shift (30,70) can result in virus escape to distant tissues, provoking systemic HR (SHR) in resistant genotypes. Occasionally, SHR will result in the death of the infected plant, a condition termed lethal SHR (LSHR) (28,29).…”

mentioning

confidence: 99%

Loss and Gain of Elicitor Function of Soybean Mosaic Virus G7 Provoking Rsv1 -Mediated Lethal Systemic Hypersensitive Response Maps to P3

Hajimorad

Eggenberger

Hill

2005

J Virol

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Rsv1, a single dominant resistance gene in soybean PI 96983 (Rsv1), confers extreme resistance against all known American strains of Soybean mosaic virus (SMV), except G7 and G7d. SMV-G7 provokes a lethal systemic hypersensitive response (LSHR), whereas SMV-G7d, an experimentally evolved variant of SMV-G7, induces systemic mosaic. To identify the elicitor of Rsv1-mediated LSHR, chimeras were constructed by exchanging fragments between the molecularly cloned SMV-G7 (pSMV-G7) and SMV-G7d (pSMV-G7d), and their elicitor functions were assessed on PI 96983 (Rsv1). pSMV-G7-derived chimeras containing only P3 of SMV-G7d lost the elicitor function, while the reciprocal chimera of pSMV-G7d gained the function.

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Lesion growth and virus localization in leaves of Nicotiana tabacum cv. Xanthi nc. after inoculation with tobacco mosaic virus and incubation alternately at 22°C and 32°C

Cited by 56 publications

References 12 publications

Resistance gene-dependent plant defense responses.

Resistance gene-dependent plant defense responses.

Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection.

Loss and Gain of Elicitor Function of Soybean Mosaic Virus G7 Provoking Rsv1 -Mediated Lethal Systemic Hypersensitive Response Maps to P3

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