Oxidative stress induction by Prunus necrotic ringspot virus infection in apricot seeds

Abstract

Prunus necrotic ringspot rvirus (PNRSV) was able to invade the immature apricot seed including the embryo. The amount of virus was very high inside the embryo compared with that present in the cotyledons. PNRSV infection produced an oxidative stress in apricot seeds as indicated by the increase in lipid peroxidation, measured as thiobarbituric acid-reactive substances. This lipid peroxidation increase was parallelled with an imbalance in the seed antioxidant enzymes. A significant decrease in the ascorbate-GSH cycle enzymes as well as in peroxidase (POX) activity took place in infected seeds, suggesting a low capability to eliminate H2O2. No changes in superoxide dismutase (SOD) or catalase activity were observed. A significant decrease in polyphenoloxidase (PPO) activity was also observed. Native PAGE revealed the presence of three different SOD activity bands in apricot seeds: a Mn-containing SOD and two CuZn-containing SODs. Only an isozyme with catalase, glutathione reductase (GR) or PPO activity was detected in both healthy and infected apricot seeds. Regarding POX staining, three bands with POX activity were detected in native gels in both healthy and infected seeds. The gel results emphasise that the drop detected in POX, GR and PPO activities in PNRSV-infected apricot seeds by kinetic analyses was also evident from the results obtained by native PAGE. The oxidative stress and the imbalance in the antioxidant systems from PNRSV-infected apricot seeds resemble the hypersensitive response observed in some virus-host interactions. This defence mechanism would inactivate PNRSV during seed formation and/or the storage period or even during seed germination. Those results can explain the decrease in seed germination and the low transmission of PNRSV by seeds in apricot trees.

Plasma membrane order and fluidity are diversely triggered by elicitors of plant defence

“…Such involvement of lipid and/or protein modifications in the increase in membrane order could be sought in our system, since the low level of ROS required to activate membrane adjustment argues in favour of a very specific, localized mechanism. Moreover, the regulation of immune responses by lipid peroxidation observed in plant cells (Polkowska-Kowalczyk and Maciejewska, 2001; Amari et al , 2007) reinforces our assumption.…”

Selective modification of rice (Oryza sativa) gene expression by rice stripe virus infection

“…Accumulation of reactive oxygen species can lead to necrotic cell death (Amari et al, 2007;Ishiga et al, 2009). Our results indicate that the transcription of genes for photosystems in the chloroplast was suppressed, whilst the genes for scavenger systems of reactive oxygen species were not affected by RSV infection.…”

Oxidative stress and antioxidative responses in plant–virus interactions

“…This virus can infect immature apricot seeds including the embryo, and this infection provokes an oxidative stress, as monitored by increases in lipid peroxidation and an imbalance in antioxidant defences, including decreases in the ASCeGSH cycle enzymes and POX activity [4] (Table 1). This oxidative response resembles an HRlike response observed in some plantevirus interactions and can be regarded as a defence mechanism to inactivate PNRSV during seed formation or even during germination as observed by the low seed germination rate and the low PNRSV transmission rate by seeds in apricot trees [4].…”

“…Also, different authors point out that decreases in GSH can be responsible for virus elicited symptom development in susceptible plants [e.g. [4,36,94,157,158]]. In that regard, it is noteworthy to mention that treatments inducing increases in GSH and/or the redox state of glutathione can decrease the virus contents and/or the symptoms even during compatible virus infections [27,29,158].…”