TMV infection

Extracts from 152 plant species, representing 46 different families, were screened for effects on tobacco mosaic virus (TMV) replication in cucumber cotyledons. Twenty species have shown enough activity to warrant further study. Several members of the Caprifoliaceae family increased virus replication. An extract of Lonicera involucrata enlarged the virus lesions in local lesion hosts and produced a thirty fold increase in virus titer, but had no effect on virus replication in systemic hosts. The active material appears to affect the virus defense mechanism of local lesion hosts. An extract of common geranium is an active virus inhibitor. It inactivates TMV and TMV-RNA (ribonucleic acid) in vitro by forming non-infectious complexes. In vivo, it also inhibited starch lesion formation in cucumber cotyledons incited by TMV infection. 

Hooft van Huijsduijnen, R.A.M., Van Loon, L.C. Bol, J.F. (1986). cDNA cloning of six mRNAs induced by TMV infection of tobacco and a characterization of their translation products. EMBO Journal, 5, 2057-61. 

Lawton, K., Ward., Payne, G., Moyer, M. Ryals, J. (1992). Acidic and basic class III chitinase mRNA accumulation in response to TMV infection of tobacco. Molecular and General Genetics (in press). 

The importance of SA in the activation of resistance was further underscored by the demonstration that otherwise resistant Arabidopsis plants become susceptible to Peronospora parasitica when phenylalanine ammonia lyase (PAL) activity is specifically inhibited by 2-aminoindan-2-phosphonic acid [77]. Since PAL catalyzes the first step in the SA biosynthetic pathway and resistance was restored in these PAL-suppressed plants by exogenous application of SA, increased susceptibility is presumably caused by a block in SA synthesis. Likewise, tobacco plants exhibiting epigenetic suppression of PAL gene expression due to cosuppression do not develop SAR in response to TMV infection [78]. In addition, these plants fail to systemically express the PR-la gene after TMV infection. 

More recently, it was shown that the volatile compound methyl salicylate, which is produced from SA in TMV-infected tobacco leaves, may function as an airborne signal for activating defense responses [96]. Since methyl salicylate is a liquid at ambient temperature, it, like SA, might also be transported through the vascular system. Once in the uninoculated leaves methyl salicylate is thought to induce PR gene expression, as well as resistance to TMV in tobacco, by first being converted back to SA. 

Acidic and basic class 111 chitinase mRNA accnmnlation in response to TMV infection of tobacco Plant Mol. 

Brishammar, S. and N. Juntti RNA-synthesizing enzymes in healthy and TMV-infected tobacco leaves. Separation and properties of enzymes catalyzing nucleotide polymerization Arch. Biochem. Biophys. 164 (1974) 218-223. 

Fritig, B. and L. Hirth Biosynthesis of phenylpro-panoids and coumarins in TMV-infected tobacco leaves and tobacco tissue cultures Acta Phytopathol. 6 (1971) 21-29. 

Photosynthesis in plants can be inhibited by many conditions, such as invasion by viral pathogens. The effects of TMV on photosynthesis are quite variable (4-6), which may reflect the different effects on photosynthesis induced by the different TMV strains. One of the key issues still to be resolved with the pathology of viral infection is what viral effect causes the expression of disease symptoms. Since TMV infection can affect leaf development and pigmentation and often plant growth, it is quite likely that a primal site of TMV infection is in the chloroplast. However, it is not known if the expression of chlorotic symptoms from TMV infection is the result of the inhibition of photosynthesis (5,7,8) or if TMV inhibits some other host process which induces symptoms and this then causes the inhibition of photosynthesis. 

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