Issue link: http://winesandvines.uberflip.com/i/122527
grapegrowing Host Cluster elongation to control bunch rot in winegrapes BY Stan Grant, Progressive Viticulture B unch rot in winegrapes has three components: the host, the pathogen and the environment.1 For bunch rot, the host is the grape cluster, the pathogen is one or more fungi, and the environment is the fruit zone within the grapevine canopy. Bunch rot fungi include both primary invaders capable of penetrating berry tissues, such as Botrytis cinerea, and secondary invaders that enter berries through damaged tissues. Sour rot also includes the bacteria Acetobacter.11 Plant pathologists represent the interactions of the three disease components in the form of a triangle (Figure 1). Grapegrowers may limit bunch rot through their influence on any of the three components of the disease triangle. The canopy environment can be influenced through management practices (shoot thinning and leaf removal) that decrease canopy density and thereby increase air movement in the fruit zone. These practices significantly lessen the potential for bunch rot.5,9,16 Exposed main cluster stem The pathogen, or fungi themselves, can be directly influenced with fungicide applications. The aforementioned canopy-management practices usually enhance the efficacy of the fungicides.20 Affecting the bunch rot host has proven more challenging in many instances. Certain wine grape varieties (Table I) are prone to bunch rot due to the compactness (high density) of the clusters.10,17 In such clusters, surface contact between adjacent berries restricts development of the protective exterior cuticle at the points of contact.12,14 Later, during ripening, the pressure exerted by expanding adjacent berries causes leakage of juice where some berries connect to their stems (pedicels). Such leakages—especially in combination with the presence of dead flower parts inside the cluster that hosts disease inoculum, and in varieties that have thin berry skins—promote bunch rot diseases.6,10,22 The tightness of the berry assemblage also restricts airflow in the cluster, which increases the internal tem- Exposed main cluster stem Pathogen Environment Figure 1. The disease triangle. perature and humidity, making the environment more conducive to disease. For some tight-cluster varieties, clones are available with looser clusters that are less prone to bunch rot. In addition, some rootstocks such as St. George and Dogridge are known to give rise to looser clusters than others. Figure 4. Flowers separated. Regulated deficit irrigation schedules, particularly when they cause early season moderate water stress in vines, limit berry size, loosen clusters and diminish humidity in canopies. Still, the extent that plant material selection and water management can mitigate disease is limited, and although they may somewhat reduce bunch rot, most tight-cluster varieties remain susceptible. Gibberellin Figure 2. Early cluster elongation (left). Figure 3. Late cluster elongation (right). Gibberellins are a group of plant hormones. In agriculture, the names gibberellin, gibberellic acid and gibb commonly refer to the GA3 gibberellin compound. It is the most active of the gibberellins and is synthesized in roots, young leaves, shoot tips, embryos, seeds and young berries.7,15 Gibberellin is involved in dormancy, differentiation of vascular tissues and elongation and growth of roots, stems and leaves. Its promotional effects on tissue growth involve increased cell wall plasticity, elongation and division. pr actica l win ery & vineya rd M AY 20 13 71