Associated gene markers for HR, ROS, and senescence-PCD in WT versus msrA3 transgenics. A substantial up-regulation of apx, cat, and sod on day 1 of darkness in WT leaves is indicative of the onset of oxidative burst, which was associated with induction of pr-1 and osm genes suggesting that HR was triggered. Relative to this WT response, the transgenics expressing msrA3 had a subdued HR and ROS response, more subdued in T26 line than T3 line, indicating a lower oxidative stress in them. Further, sag12, vpe, lag1 and gs-1 transcripts were less abundant in the transgenics as compared to the WT, but opposite trends of accumulation were apparent for rbcL transcripts. These results together with differential loss of chlorophyll content and visual observations suggest that msrA3 expression antagonizes or delays apoptosis in transgenics compared to the WT. The dampening effect of msrA3 expression on gene markers for HR, ROS and PCD-senescence in the transgenic lines was also evident during challenge with the necrotrophic pathogen F. solani. MsrA3 as an antimicrobial agent effectively prevented necrosis in the leaves of transgenic potato Orbifloxacin plants in Mepiroxol response to the pathogen challenge compared to the WT leaves. Consistent with the phenotypic observations, the transgenic leaves had subdued induction of pr-1 and osm gene transcripts compared to their robust induction in the WT leaves within day 1 of pathogen inoculation. Since these genes in potato tubers form a part of hypersensitive defense response against this fungus, it is evident that msrA3 expression interferes with the pathogen-mediated HR. The suppressive effect of the msrA3 expression on HR induction was further supported by the pattern of induction or lack thereof of cat and apx gene transcripts in the transgenics. In this regard, selective activation of vpe and gs-1 only in the leaves of WT plants highlights F. solani-mediated cell death pathway, which is clearly mitigated in msrA3-expressing transgenic plants. In addition to its role in senescence, vpe is considered as one of the architects of virus-induced HR and cell death. It is worth noting that vpe expression was more enhanced in F. solani challenged WT leaves than during their dark-induced senescence. Cell death is a culmination of defense response, which is relatively more rapid and intense in response to a pathogen than during senescence. Similar trend in the activation of gene transcripts was evident in the neighboring non-inoculated leaves, which is reminiscent of the systemic response. Again, except for a subdued induction of pr-1 and cat gene transcripts, expression of the remainder of the tested genes was nearly absent in the inoculated and neighboring leaves of the msrA3 transgenic plants. The synthetic activity of peroxidases produces, dismutated by SOD to H2O2. Induction of the potato peroxidase, Stprx2, which is more of an anabolic peroxidase rather than H2O2 catabolizing enzyme due to its similarity with peroxidases involved in oxidative burst, in conjunction with sod transcripts during wounding and pathogen challenge in leaves of WT plants is suggestive of its involvement in oxidative burst in potato. These results also favor the possibility that msrA3 expression intercepts normal plant defense response including ROS, HR and senescence, which in turn may contribute to the lower threshold of ROS homeostasis in the growing plants. Independent or co-induction of salicylic acid, JA and/or ethylene is considered a common defense response of plants against pathogen attack or abiotic stressors, and likely culminates in cell death processes involving ROS. SA increases in response to biotrophs and JA in response to necrotrophs and insects. Wounding induces synthesis of JA, ethylene and SA. Also, a selective involvement of JA and SA has been indicated based on the wounding agent employed.