First attempts to discriminate between tapping panel dryness (TPD) and bark necrosis (BN), two Hevea sp. bark diseases leading to the cessation of latex production, showed differences in latex biochemical characteristics (1). Further, contrary to TPD, BN is characterized by inner phloem necrosis starting at the rootstock/scion junction (RS/S) and spreading upward to the tapping cut. Recent etiological (3) and epidemiological studies did not provide evidence of a causative pathogen for BN, but showed that BN is favored by a combination of various stresses (2). Searching for molecular markers of BN using sodium dodecyl sulfate-polyacrylamide gel electrophoresis analyses highlighted differential expression of some proteins in the latex and bark, especially a 67-kDa protein, which accumulates in the inner phloem of the BN trees. This protein was identified by peptide microsequencing as a linamarase (cyanogenic β-glucosidase). This led to the suspicion of the involvement of cyanogenesis in the spread of the syndrome inside the inner bark. The cDNAs of enzymes involved in cyanide (CN) metabolism (linamarase, hydroxynitrile lyase, and cyanoalanine synthase) were cloned from our Hevea sp. phloem specific cDNA library. In addition, the most BN-susceptible rubber clones were shown to exhibit higher cyanide potentions in the leaves and bark, together with low cyanoalanine synthase (CAS) gene expression and activity. Furthermore, linamarine (the cyanogene glucoside substrate of linamarase) was shown to accumulate in the phloem at the base of the trunk, especially above the rootstock/scion junction. The results of biochemical and gene expression studies associated with recent ecophysiological advances (2) strongly suggest a possible cell decompartmentalization near the RS/S junction, resulting in a local release of toxic concentration of highly diffusive CN. This, combined with a lethal imbalance between cyanogenic and CN-detoxifying activities (CAS) in the phloem of BN trees, could lead to poisoning of neighboring cells and to the spread of tissue necrosis toward the tapping cut. In conclusion, after providing evidence of exogenous factors favoring BN (2), this report highlights endogenous disorders that may be at the origin of this physiological disease leading to BN.
References: (1) D. Nandris et al. Eur. J. For. Pathol. 21:325, 1991. (2) D. Nandris et al. Plant Dis. 88:1047, 2004.
