The Timing of Senescence and Response to Pathogens Is Altered in the Ascorbate-Deficient Arabidopsis Mutant vitamin c-1  

Abstract

The ozone-sensitive Arabidopsis mutant vitamin c-1 (vtc1) is deficient in l-ascorbic acid (AsA) due to a mutation in GDP-Man pyrophosphorylase (Conklin et al., 1999), an enzyme involved in the AsA biosynthetic pathway (Smirnoff et al., 2001). In this study, the physiology of this AsA deficiency was initially investigated in response to biotic (virulent pathogens) stress and subsequently with regards to the onset of senescence. Infection with either virulent Pseudomonas syringae or Peronospora parasitica resulted in largely reduced bacterial and hyphal growth in the vtc1 mutant in comparison to the wild type. When vitamin c-2 (vtc2), another AsA-deficient mutant, was challenged with P. parasitica, growth of the fungus was also reduced, indicating that the two AsA-deficient mutants are more resistant to these pathogens. Induction of pathogenesis-related proteins PR-1 and PR-5 is significantly higher in vtc1 than in the wild type when challenged with virulent P. syringae. In addition, the vtc1 mutant exhibits elevated levels of some senescence-associated gene (SAG) transcripts as well as heightened salicylic acid levels. Presumably, therefore, low AsA is causing vtc1 to enter at least some stage(s) of senescence prematurely with an accompanying increase in salicylic acid levels that results in a faster induction of defense responses.

Modulation of host plant immunity by Tobamovirus proteins

“…gmp1 silenced plants produced enhanced levels of ROS and reduced TMV accumulation. In agreement with this, previous reports had shown that reduced levels of GMP1 were associated with augmented basal defences mediated by SA and pathogenesis-related (PR) protein expression in A. thaliana (Barth et al, 2004;Pavet et al, 2005). Conti et al (2012) demonstrated that gmp1 silenced N. benthamiana plants also displayed an increased accumulation of PR proteins.…”

Cooperative Ethylene and Jasmonic Acid Signaling Regulates Selenite Resistance in Arabidopsis

“…It has been reported that extreme levels of ROS can trigger the production of SA that in turn leads to more ROS via a self-amplifying loop, activating the oxidative cell death cycle (Overmyer et al, 2003;Kangasjärvi et al, 2005). Indeed, a previous study showed that the vtc1 mutant produces high levels of SA after inoculation with a pathogen (Barth et al, 2004). To assess whether a high level of SA was also present in the selenite-treated vtc1 mutant, we carried out semiquantitative RT-PCR to evaluate the expression of the PR1 gene, which encodes the SAresponsive PR1, which is frequently used as a marker for SA signaling (Cao et al, 1997).…”

Mobilization of Rubisco and Stroma-Localized Fluorescent Proteins of Chloroplasts to the Vacuole by anATGGene-Dependent Autophagic Process

“…cDNA from 0.3 mg of total RNA was used as template for each 100-mL PCR. Gene-specific primers used for PCR were 5#-ACCTTCTCCGCAACAAGTGG-3# and 5#-GAAGCTTGGTGGCTTGTAGG-3# for RBCS2B (Acevedo-Hernández et al, 2005), 5#-CAGCTTGCCCACCCATTGTTA-3# and 5#-GTCGTACGCA-CCGCTTCTTTCTTA-3# for SAG13 (Barth et al, 2004), and QuantumRNA 18S internal standards for 18S ribosomal RNA (Ambion). PCR was terminated after 12 cycles for RBCS2B, 18 cycles for 18S ribosomal RNA, and 26 cycles for SAG13.…”