Internal Heat Necrosis of Potato—A Review

Abstract

Non-pathogenic necroses of potato tubers have been described in the literature since the early 20th century using different names including internal rust spot, internal browning, physiological internal necrosis, internal brown fleck, chocolate spot, internal brown spot and internal heat necrosis. These reports very likely describe either the same, or a collection of similar disorders, falling under the general umbrella of “internal necrosis”, with the expression of symptoms being significantly altered via genotype by environment interactions. A number of widely-grown cultivars (e.g. ‘Russet Burbank’, ‘Atlantic’ and ‘Yukon Gold’) are susceptible to internal necrosis, making it an economically significant problem. In Atlantic, this syndrome has been termed internal heat necrosis (IHN) in the eastern United States by several investigators because heat and drought are believed to be important triggers of this condition. Investigators in the midwestern and western United States term this same or similar disorder internal brown spot (IBS). IHN and IBS are an internal physiological disorder of potato characterized by brownish red necrotic patches of parenchymal tissue that typically, though not always, occur along and/or inside the vascular ring. Several reports indicate that IHN is most commonly associated with the vascular ring tissue near the apical end of the tuber, but IHN may form anywhere in the tuber. In many cases, it is very difficult to distinguish between IHN and IBS, and several overlapping environmental factors are associated with each of these disorders. High day and night temperatures early in the growing season, combined with low rainfall, have been shown to increase the frequency and severity of IHN and IBS in several cultivars. Considerable research has examined the role of calcium in ameliorating IHN and IBS expression. Much of this work suggests an important role for calcium in the development of IHN, but other biotic and abiotic factors undoubtedly affect IHN and IBS expression. The biochemistry and genetics behind internal necroses of potato have historically been the least-researched facets of this problem. Research has shown that enzymes involved in protecting cells from oxidative damage may be involved, and heritability studies have demonstrated that broad-sense heritability for IHN resistance is high. This review seeks to outline previous work on physiological internal necroses of potato due to high temperatures, summarize our current knowledge of IHN, and point to new areas of investigation to develop IHN resistant potato varieties.