Sunburn in Grapes: A Review

Abstract

Sunburn is a physiological disorder that affects the visual and organoleptic properties of grapes. The appearance of brown and necrotic spots severely affects the commercial value of the fruit, and in extreme cases, significantly decreases yield. Depending on the severity of the damage and the driving factors, sunburn on grapes can be classified as sunburn browning (SB) or as sunburn necrosis (SN). Sunburn results from a combination of excessive photosynthetically active radiation (PAR) and UV radiation and temperature that can be exacerbated by other stress factors such as water deficit. Fruit respond to these by activating antioxidant defense mechanisms, de novo synthesis of optical screening compounds and heat-shock proteins as well as through morphological adaptation. This review summarizes the current knowledge on sunburn in grapes and compares it with relevant literature on other fruits. It also discusses the different factors affecting the appearance and degree of sunburn, as well as the biochemical response of grapes to this phenomenon and different potential mitigation strategies. This review proposes further directions for research into sunburn in grapes.

Keywords: ROS; antioxidants; mitigation; photooxidation; sunburn browning; sunburn necrosis.

Figure 1

Sunburn necrosis (SN) of Bacchus, a highly susceptible grape variety in the field after bunch zone defoliation.

Figure 2

Images of Chardonnay bunches with increasing degrees of sunburn browning (SB; A–C, 0–51%) and SN (D–F, 12–32%) damage. Pictures were taken at harvest (~22°Brix) in Orange, Australia.

Figure 3

Rachis damage caused by SN in Riesling. 47% of berries were damaged due to a sunburn event occurring on July 25, 2019. Picture was taken on September 30, 2019, at 19.5°Brix in Geisenheim, Germany.

Figure 4

Infrared and RGB pictures of grape berries heated with an infrared heat emitter. The temperature gradients induced by IR heating allow for the determination of threshold temperature for the appearance of necrotic spots. In this example, detached ripe Sultana grapes (19.3°Brix) suffered SN damage at 52°C.

Figure 5

Epidermal cell, photoprotection, and reactive oxygen species (ROS) scavenging mechanisms. As photosynthetically active radiation (PAR) and UV light reach the berry, part of these forms of radiation are reflected by the cuticle. Vacuolar phenolics (A) act as a screen helping to reduce the amount of incident light further penetrating the cell and help mitigate part of the ROS formed through the formation of oxidized phenolic forms and complex brown polymers (if ascorbic acid is absent). If light penetrates further into the hypodermis, the chloroplasts and mitochondria become the main target of radiation. The water-water cycle (B), non-photochemical quenching (NPQ; C), and tocopherol (D) are used to remove ROS and prevent damage to the photosystems. AA, ascorbic acid; DHA, dehydroascorbate; MDHA, monodehydroascorbate; DHAR, dehydroascorbate reductase; APX, ascorbate peroxidase; SOD, superoxide dismutase; GSSG, glutathione disulfide; GSH, glutathione; GR, glutathione reductase; PSI, photosystem I; POX, polyphenol oxidase; PPO, polyphenol peroxidase; POH, polyphenol; PQ, oxidized phenol; VDE, violaxanthin de-epoxidase; ZE, zeaxanthin epoxidase. Based on Solovchenko and Merzlyak (2008).

Figure 6

Carotenoid synthesis is up-regulated in response to changes in the light environment. As a consequence of higher light, α‐ and β-carotene are synthesized from lycopene and used to produce more lutein and violaxanthin. The violaxanthin cycle is rapidly induced in response to high light, and violaxanthin is epoxidized first to anteraxanthin and then to zeaxanthin. Violaxanthin de-epoxidase (VDE) requires ascorbate (AsA) and a pH gradient to catalyze the reaction. In the absence of ascorbate, zeaxanthin is converted to neoxanthin. The lutein epoxide cycle converts lutein epoxide into lutein and is induced when tissues move from a shade to normal light situation or under prolonged high light stress.

Figure 7

Schematic representation of the responses of grapes to abiotic stress. Plants are initially in a basal state when stress is applied. Stress can be divided into lethal stress (red lines) which lead to acute damage and cell death; and sub-lethal stress (green line) which leads to the activation of a series of stress response mechanisms. Prolonged stress (purple line) leads ultimately to chronic damage and cell death. If sufficient recovery time is allowed, fruit returns to the original basal state (green dotted and dashed lines).

Figure 8

Scanning electron micrographs (×2000 magnification) of epicuticular waxes of Chardonnay grapes. (A) Control grapes with no sunburn; (B) slight sunburn; (C) moderate sunburn; (D) severe sunburn (originally from Greer et al., 2006; reprinted with permission from Vitis).

Figure 9

Thermal images of Riesling bunches on the two canopy sides of N-S, NE-SW, and E-W row orientations during the course of the day, taken on August 26, 2012, in Geisenheim, Germany.

Figure 10

Uneven berry development induced by light and heat overexposure in Cabernet Sauvignon with minimal sunburn damage (0–3%). (A) Eastern side of four bunches showing normal development. (B) Western side of the same bunches, showing delayed color change, smaller berries (mean: 1.04 vs. 1.29 g), and a delayed sugar accumulation (mean: 8.7 vs. 15.2°Brix). Images were taken on August 24, 2020, in Geisenheim, Germany, after a pre-véraison heatwave that occurred from August 7, 2020 to August 12, 2020.