Physiological Disorders in Tomato Fruit Development

Physiological disorders are abnormalities in fruit color or appearance that are abiotic in origin. These abnormalities are often confused with damage from pathogens or insects (biotic damage). Physiological disorders are distinguished from deficiencies of a single nutrient, and physical, chemical or herbicide injury. Causes of physiological disorders include genetic susceptibility, environmental factors, watering practices, nutrition, and cultural practices such as pruning and training. For most physiological disorders, a number of factors are involved, and there is almost always a genetic component. This complex interplay of factors is poorly understood for most disorders, and in some cases contradictory results have been reported. There are also a number of different names for many disorders. Although there are many interactions, for the purposes of this discussion, physiological disorders are divided into groups: nutrient imbalances, especially between potassium and nitrogen or magnesium (blotchy ripening, greywall); calcium amount or movement into the fruit (gold fleck or speck, blossom-end rot); temperature extremes (catfacing, boat fruit, rough fruit, puffiness, sunscald); genetic predisposition (green or yellow shoulder) and watering (cracking, russeting, rain check, shoulder check). Secondary effect of pathogens or insects (ghost spot from Botrytis, dimpling from thrips, uneven ripening from silverleaf whiteflies, patterning as a result of tomato spotted wilt or pepino mosaic virus) can also be considered physiological disorders, but are not reviewed here since the cause is biotic. INTRODUCTION The disorders discussed below have both genetic and environmental components, and in many cases the exact cause of the disorder is not well understood or involves a complex of factors. Thus, although the discussion is divided into separate categories in almost all cases more than one factor or category is involved. Physiological disorders covered in this review have a characteristic set of symptoms whose origin cannot be attributed solely to a biological agent or to a single environmental or cultural factor. The following discussion does not include descriptions of nutrient deficiencies, air pollution damage, herbicide injury or chilling injury. Secondary effects of pathogens or insects (ghost spot from Botrytis, dimpling from thrips, uneven ripening from silverleaf whiteflies, patterning as a result of tomato spotted wilt or other virus) can also be considered physiological disorders, but are not reviewed here since the cause is biotic. For many physiological disorders, little in-depth research has been done and the cause is poorly understood both in terms of why cultivars differ in susceptibility and why certain environments or cultural practices predispose plants to the disorder. Physiological disorders have been reviewed by Kinet and Peet (1997), Dorais and Papadopoulos (2001), Dorais (2001), Gruda (2005), Peet (2005), and Savaas et al. (2008). Proc. IS on Tomato in the Tropics Eds.: G. Fischer et al. Acta Hort. 821, ISHS 2009 152 NUTRIENT IMBALANCES Blotchy Ripening Complex Of all the physiological disorders of tomato, the ripening disorders (blotchy ripening, greywall and internal browning) are the least understood. There is disagreement over whether ripening disorders are physiological, biotic or genetic in origin and whether symptoms represent distinct disorders or different manifestations of the same disorder. Similar fruit symptoms appear on plants infected with certain viruses, but in this case leaves will normally also show symptoms (Savvas et al., 2008). Dorais et al. (2001) reported an increase in uneven fruit coloring/blotchy ripening under low light. Fruit deficient in potassium are more susceptible to blotchy ripening, grey wall, and may lack good fruit coloration. Plants growing under optimal conditions and carrying high fruit loads can take up to 140-230 mg potassium per day from the nutrient solution. In contrast, only 80-110 mg of nitrogen and 22-35 mg phosphorus per plant per day are taken up (Morgan, 2006). Thus maintaining high potassium in the fruit is particularly challenging (Morgan, 2006). All that can be said to generalize about ripening disorders is: 1) cultivars differ in susceptibility; 2) the incidence increases when potassium is low and decreases when potassium is raised; 3) affected areas of the fruit eventually show signs of tissue necrosis, usually involving the vascular system; and 4) affected areas are usually lower in soluble solids and titratable acidity, decreasing fruit quality. Usually fruit with ripening disorders are unmarketable. CALCIUM-RELATED DISORDERS Blossom-End Rot (BER) 1. Description. At the anatomical level, the earliest symptoms are areas of white or brown locular tissue. Symptoms next appear in the fruit placenta in the case of internal blossom-end rot or in the blossom-end pericarp in the case of external blossom-end rot (Adams and Ho, 1992). Externally, the disorder begins as a small, water-soaked spot at or near the blossom scar of green tomatoes. As the spot enlarges, the affected tissue dries out and turns light to dark brown, gradually developing into a well-defined, sunken, leathery spot. Internal BER, consisting of black necrotic tissues in the parenchyma around the young seeds and the distal placental tissues (Adams and Ho, 1992) often develops in the same fruit. 2. Causes. Interactions between daily irradiance, air temperature, water availability, salinity, nutrient ratios in the rhizosphere, root temperature air humidity and xylem tissue development in the fruit all contribute to BER incidence (Dorais and Papadopoulos, 2001). Although BER shows up in distal fruit tissue, and a gradient in fruit calcium concentration has been shown (Adams and Ho, 1992), Dorais and Papadopoulos (2001) cited evidence that calcium content and cation distribution within the fruit is not directly related to BER. Ho et al. (1993) reported a positive relationship between BER incidence and the product of the average daily solar radiation integral and temperature during the period of rapid fruit growth. They separated high light and high temperature effects from each other in a series of greenhouse experiments in which the effects of raising temperatures by 2°C were compared to those of shading to reduce light. Added heating was found to increase BER incidence to a much greater extent than added sunlight, presumably because high temperatures increase the rate of fruit expansion more than does extra light. A rapid rate of fruit enlargement (Ho et al., 1993) would increase the demand for calcium in plasmalemma synthesis because of the higher rate of cellular enlargement. This may explain the observation of DeKock et al. (1982a) that thinning tomatoes to 1 or 2 fruit per truss increases the size of the fruit at first but subsequent trusses were severely affected by blossom-end rot. Dorais and Papadopoulos (2001) summarize the work of Ho and coworkers by concluding that lack of coordination between accelerated cell enlargement, due to high import of assimilates, is generally linked to fruit susceptibility to BER when