Abstract
CIP-29, a basic glycoprotein purified from the leaves of Clerodendrum inerme, induces resistance against viruses in plants. It is a type-I ribosome-inactivating protein (RIP) with polynucleotide:adenosine glycosidase activity. Present study was made to compare the resistance induced against TMV by CIP-29 and salicylic acid (SA), a chemical elicitor of systemic acquired resistance (SAR). Foliar treatments with CIP-29 (20 µg mL(-1)) and SA (2.5 mM) on Nicotiana tabacum cv. Xanthi-nc resulted in a percent reduction of TMV lesion number by 99 and 64 on remote leaves and decrease in lesion diameter by 2.67- and 1.97-fold, respectively. CIP-29-treated (resistant) tobacco leaf extract inhibited TMV by 93%, as against 25% by SA, suggesting induction of a virus inhibitory agent (VIA) in the former. In semi-quantitative gene expression analysis of treated and inoculated (+V) sets of tobacco Xanthi-nc, PR1a (PR-1) and Osmotin (PR-5) gene transcripts were significantly enhanced only in SA-treated set, and showed pronounced accumulation in both CIP-29+V and SA+V. Acidic chitinase (PR-3) transcripts were detectable only in SA and SA+V. Expression of allene oxide cyclase (AOC) gene was prominent in CIP-29+V and DW+V, while 1-aminocyclopropane-1-carboxylate oxidase (ACO) and ethylene responsive factor 1 (ERF1) genes were expressed in greater intensity in CIP-29+V. In qPCR analysis of ACO and ERF1 genes, a respective fold increase of 377.4 and 25.1 was observed in the post-inoculated CIP-29-treated sets compared to an increase by 22.5- and 10.2-fold in SA-treated sets. Between 14 and 28 days post-inoculation with TMV, symptomatic plants of Solanum lycopersicum increased from 0 to 20% in the CIP-29 treated set, compared to an increase from 30 to 90% in SA-treated set. Greater delay in symptom progression and accumulation of TMV was noted in CIP-29 compared to SA-treated sets, while growth parameters were significantly higher following SA treatment. This study clearly points to different mechanisms governing phytoprotein and chemical induced resistance.