Water — Too much water decreases inflorescence; water deficit does not.4 The affect of over-watering is thought to be indirect; water encourages excessive canopy growth, which shades the canes and draws carbohydrates away from the buds. Irrigation maintaining between 60% and 80% of full ET maximized bud fruitfulness.4

Nitrogen — Nitrogen deficiency reduces fruitfulness.2 On the other hand, too much nitrogen causes rapid shoot growth, which will pull carbohydrates away from the buds and reduce their fruitfulness.

Mineral deficiencies — There is some evidence that lack of phosphorus or potassium reduces bud fruitfulness.2 Low phosphorus around bud break is sometimes caused by cold soil that prevents uptake by the roots, even if the soil has enough of themineral. Potassiumor phosphorus can be added by foliar sprays. The applications would need to be shortly after bud break to increase fruitfulness in the first several buds. No experiments have yet been performed to test this idea.

Plant growth regulator compounds — Plants regulate inflorescence by the interaction of gibberrellic acid (GA) and cytokinins.4 At an early stage, GA increases inflorescence by favoring formation of anlage. But later, GA decreases inflorescence by favoring the alternative path to tendril formation.2,4 Cytokinins increase inflorescence by favoring inflorescence over tendrils. They also regulated flower differentiation just before budbreak.4

Cytokinins are produced naturally in the plant, and they can be augmented with kelp sprays. It might be worthwhile to experiment with kelp in blocks with low fruitfulness, or in years with cold spring weather. Kelp has not been proven to contain the correct cytokinins for grapes; more research is needed.

Adding too much gibberellin can reduce inflorescences,2 but gibberellin is not normally applied soon after bud break. It is more important during the necrosis period, after bloom.

Plant-mediated bud necrosis. The primary bud is dead above an abscission layer.

In plant-mediated bud necrosis (PMBN), the middle section of the primary bud dies above an apparent abscission layer. Presumably the necrosis is initiated by some plant hormone. The dead section rather quickly turns into brown fluff that breaks away from the bud when pushed. The two secondary buds usually survive. This kind of necrosis is often called primary bud necrosis (PBN), but injury can also cause necrosis of primary buds (see photo, page 13).

The few studies investigating PMBN indicate that it usually occurs during the first one or two months following bloom. During this time, carbohydrates are flowing preferentially to the current season’s flower clusters and young berries, leaving less for the developing buds.

Carbohydrate shortage, shading, shoot vigor, and excessive gibberellin have been shown to promote PMBN.

Low carbohydrates — Many studies point to the role of a low level of carbohydrates in PMBN. Buds with lower carbohydrate levels are more likely to die. More vigorous shoots tend to have less carbohydrates and more necrosis than weaker shoots. Grape varieties that tend to have more carbohydrates also tend to be more resistant to PMBN.5,6

A study in Virginia found more PMBN in several varieties with low carbohydrates (Riesling, Syrah, and Viognier) than in one with high carbohydrates (Chardonnay).6

By the time PMBN starts, after bloom, the carbohydrate contribution of the leaves is presumably more important than reserves in the wood and roots. In a healthy vine, the leaves will be supplying new reserves, in addition to growing the current year’s fruit, andmaintaining next year’s buds.