ANATOMY OF CHLOROTHALONIL-INDUCED GRAPE BERRY RUSSET

Clusters of Vitis labruscana cv. Concord were grown either in full sun or canopy shade, and either not sprayed or sprayed with 3.4 Kg/Ha chlorothalonil every 2 wk from pre-bloom to veraison. Only sun-exposed, sprayed fruit produced skin russeting. Clusters of the very susceptible V. vinifera cv. Rosette were grown in direct sun, sprayed with chlorothalonil 4 times from bloom to veraison, in the presence or absence of purported anti-russeting agents. Heavy russet occurred in all treatments. Russet initiation was similar in the 2 cvs.: epidermal cells first died beneath spray residue in full sun, a phellogen then arose in the hypodermis, followed by periderm. Epidermal death began in `Rosette' within a wk of the bloom spray, but in `Concord' only after 2-3 wk post bloom and 3 sprays. `Concord' russet generally appeared as patches or scabs, whereas `Rosette' russet ranged from freckles, welts, scabs to large smooth burnished areas. In both cvs., unbroken russet consisted of uniform layers of phellum. New, deeper periderm initials arose beneath checks and cracks which formed as fruit enlarged. In `Concord', but not `Rosette', the daughter cells of each such initial were often enclosed in the original cell wall. In all cases of russet, cell walls in the periderm were suberized and sometimes lignified. Cells also contained much phenolic material.