A series of experiments was carried out on Pinot noir grapevines to better understand flower necrosis. Previous research on late bunch stem necrosis indicated that accumulation of putrescine was the causal agent. It has been assumed that putrescine also causes flower necrosis, but this has not been confirmed. We tested whether putrescine accumulation causes flower necrosis by supplying various metabolites, including agmatine, to single-node flower cluster cuttings or by applying metabolites to developing clusters via a needle-delivery method in the field. Both approaches showed that high levels of putrescine in the rachis can cause flower necrosis and induce pedicel abscission in the field. The concentration of putrescine that induced flower necrosis in the field was similar to previous work on late bunch stem necrosis. However, further work comparing healthy and necrotic clusters from Pinot noir grapevines grown in sand-culture (with a history of flower necrosis) showed that flower necrosis was not due to accumulation of putrescine. These findings, combined with other field observations, led to the hypothesis that flower necrosis may also be caused by an imbalance in the root to shoot ratio of vines. This hypothesis was tested by manipulating shoot number in the sand-culture vines and in other vines with no prior history of flower necrosis. In both, flower necrosis correlated with lower shoot density per vine. In addition, root pruning of vines partially reversed the impact of low shoot density on flower necrosis. These findings show that while putrescine can induce flower necrosis in artificial experiments, another, presently unknown mechanism related to coordinated root and shoot development (and/or transport and sensing) causes flower necrosis in the field. Vineyard blocks with a history of flower necrosis could be improved by increasing shoot density or limiting root development.

Funding Support: USDA-ARS