Enzyme-mediated metabolism in nutritive tissues of galls induced by Ditylenchus gallaeformans (Nematoda: Anguinidae)

The galls induced by Ditylenchus gallaeformans (Nematoda) on leaves of Miconia albicans have unique features when compared to other galls. The nematode colonies are surrounded by nutritive tissues with promeristematic cells, capable of originating new emergences facing the larval chamber, and providing indeterminate growth to these galls. Considering enzyme activity as essential for the translocation of energetic molecules from the common storage tissue (CST) to the typical nutritive tissue (TNT), and the major occurrence of carbohydrates in nematode galls, it was expected that hormones would mediate sink strength relationships by activating enzymes in indeterminate growth regions of the galls. Histochemical, immunocytochemical and quantitative analyses were made in order to demonstrate sites of enzyme activity and hormones, and comparative levels of total soluble sugars, water soluble polysaccharides and starch. The source-sink status, via carbohydrate metabolism, is controlled by the major accumulation of cytokinins in totipotent nutritive cells and new emergences. Thus, reducing sugars, such as glucose and fructose, accumulate in the TNT, where they supply the energy for successive cycles of cell division and for nematode feeding. The histochemical detection of phosphorylase and invertase activities indicates the occurrence of starch catabolism and sucrose transformation into reducing sugars, respectively, in the establishment of a gradient from the CST towards the TNT. Reducing sugars in the TNT are important for the production of new cell walls during the indeterminate growth of the galls, which have increased levels of water-soluble polysaccharides that corroborate such a hypothesis. Functional relationship between plant hormone accumulation, carbohydrate metabolism and cell differentiation in D. gallaeformans-induced galls is attested, providing new insights on cell development and plant metabolism.