Abstract

Examination of `Riesling' grape (Vitis vinifera L.) in Virginia suggested that a high incidence of bud necrosis (BN) in some vineyards was associated with canopy shade and rapid shoot growth. BN appeared to originate as an abortion and dehydration of the primary, and occasionally secondary, buds of the developing dormant bud. BN frequency was lowest among the basal four nodes of a given shoot or cane, and increased in frequency through node 20. Experiments were conducted in 1991 and 1992 to evaluate the specific involvement of shoot growth rate and canopy shade on `Riesling' BN. Shoot growth rate (SGR), measured in a 17-day period around bloom, had a significant, positive relationship with BN in one of two vineyards. BN was positively associated with cane diameter and average internode length. Applying the growth retardant paclobutrazol significantly reduced SGR and BN incidence up to 80% among nodes 6 to 15 in two separate vineyards. Artificial shade (64% or 92% reduction in photosynthetic photon flux), suspended over vine canopies in the 3-week period before véraison, did not affect BN. Shoots of canopies that had been thinned before bloom to 10 shoots/m of canopy expressed slightly lower BN levels than shoots sampled from canopies that had been thinned to 20 shoots per meter. `Riesling' BN appeared more influenced by shoot vigor than shade under Virginia growing conditions. Chemical name β-[(4-chlorophenyl)methyl]-α-(1,1-dimethyl-ethyl)-1H-1,2,4-triazole-1-ethanol (paclobutrazol).

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