A mineral element is considered as essential, when plants cannot complete reproductive stage of life cycle due to its deficiency. Deficiency must be corrected only by supplying the element in question and when the element is directly involved in the metabolism of the plant (Arnon, 1954). Based on these criteria, sixteen elements so far were identified as essential. These are: carbon, hydrogen, oxygen, nitrogen, phosphorus, potassium, calcium, magnesium, sulphur, iron, manganese, zinc, copper, boron, molybdenum and chlorine. Most of the carbon as carbon dioxide enters the plant from the air; hydrogen and oxygen are taken up as water. The rest of the elements are taken up from the soil solution as mineral nutrients. Among these nutrients N, P, K, Ca, Mg, and S are considered major or macro-nutrients, because they are required in large quantities that range between 1 to 150 g per kg of plant dry matter. Fe, Zn, Mn, Cu, B, Mo and Cl are minor or micro-nutrients that are required at rates of 0.1 to 100 mg per kg of plant dry matter (Marschner, 1997a). Chloride is essential in micro quantities but can accumulate in the plant in large quantities when present in high concentrations in the soil solution, (Xu et al., 2000).
All the essential nutrients are required by plants in balanced proportions. Deviation from this may result in nutritional disorders. Early detecting of nutritional deficiency stress is important. Stress might extend to the entire plant with loss of yield if relief of stress is not employed. Continuous shortage of a nutrient or nutrients might cause plant death. When two or more elements are deficient simultaneously, the composite picture of symptoms may resemble no single known deficiency. Mineral deficiency symptoms are sometimes confused with other complex field events such as damage caused by insect-pest, disease, salt stress, water stress, pollution, light and temperature injury (Bennett,1993) and herbicide damage. Toxicity of Mo or Se is similar to P deficiency (Bennett, 1993), Fe deficiency in Mango is similar to Chloride toxicity (Xu et al., 2000). Therefore, it is necessary to critically observe and define these deficiency symptoms. The deficiency symptoms might be distinguished based on the plant part that shows deficiency symptoms, presence or absence of dead spots and entire leaf or interveinal chlorosis. A description of initial appearance of deficiency symptoms on leaves is given in Fig.1 and the associated text below. Generally, nutrient deficiency in the plant occurs when a nutrient is insufficient in the growth medium and/ or cannot be absorbed and assimilated by the plants due to unfavourable environmental conditions. Nutrient disorders limit crop production in all types of soil around the world. Table 1 shows soil conditions associated with nutrient deficiencies of various nutrient elements.
Visual symptoms of nutrient deficiency – Photos http://www.hbci.com/~wenonah/min-def/list.htm
Boron deficiency causes yellowing or chlorosis of youngest leaves and stems (Yu et al., 1998) which starts from the base to the tip. Rosetting of terminal shoots of potato (Roberts and Rhee, 1990). Leaf tip burn, elongate and become whitish brown in rice (Yu et al., 1998). Death of terminal bud occurs in extreme cases. Boron deficiency causes brown heart in radish (Shelp et al., 1987) and crown choking in coconut (Baranwal et al., 1989).
Calcium stress in plants results in chlorosis of young leaves along the veins of birdsfoot trefoil (Russelle and McGraw, 1986) and blueberry (Tamada, 1989), if deficiency persist longer, bleaching of upper half leaf followed by leaf tip curling do occur in black pepper (Nybe and Nair, 1987) and sugarcane (Nautiyal et al., 2000). The growing bud leaf becomes chlorotic white with base remaining green, the distortion of the tips of shoots i.e. dieback was observed by Edwards and Hortan, (1997) in peach seedlings. Similarly, Spehar and Galway, (1997) found brown spots on leaves, reduced expansion and premature leaf senescence under Ca stress in soybean crop. Stress during fruiting in tomato increases susceptibility to blossom end rot (Adams and El-Gizawy, 1988; Sonneveld and Voogt, 1991 and Ho et al., 1999). Calcium stress is also responsible for other disorders such as bitter pit in apple (Ford, 1979; Monge et al., 1995 and Silva and Rodriguez, 1996); leaf tip burn in cabbage (Miao et al., 1997) and lettuce; black heart of celery; cavity spot of carrots (Scaife and Clarkson 1978); vitrescence in melons (Jean-Baptist et al., 1999).
The symptoms of chlorine deficiency develop first on the older leaves. Discrete patches of pale green chlorotic tissue appear between the main vein near the tip of the leaf, downward cupping of some of the older leaves of Kiwifruit was observed by Smith et al., (1987). The leaflets of youngest leaves shrivel completely, older leaflets develop a brown necrosis which start near the tip and extend backwards particularly at the margins of red clover (Whitehead, 1985).
In copper deficiency, visible foliar symptoms appear on young leaves as chlorosis changing to necrosis (Conover et al., 1991; Del, 1994); rolling, wilting and twisting of leaves in wheat (Owuoche, 1995). The later affected leaves appear papery and twisted in rice (Nautiyal et al., 1999 ).
The principal veins remain conspicuously green and surrounding portion of the younger leaves turn yellow tending towards whiteness in chickpea (Mehrotra and Gupta, 1990 and Saxena et al., 1990); groundnut (Reddy et al., 1993); radish, cauliflower, cabbage and sorghum (Preeti et al., 1994); lentil (Zaiter & Ghalayini, 1994) and soybean (Fonts and Cox, 1998). Under severe deficiency, most part of the leaf becomes white (Russelle and McGraw, 1986 ).
Magnesium deficiency causes yellowing, but differs from that of nitrogen. The yellowing takes place in between veins of older leaves (Makkanen, 1995) of Picea abies and veins remain green, this is followed by necrosis of tissues in birdsfoot trefoil (Russelle and McGraw, 1986), melons (Simon et al., 1986). black pepper (Nybe and Nair, 1987) and blueberry (Tamada, 1989). Mg deficiency my be induced in tomatoes by high levels of ammonium in the nutrient solution (Kafkafi et al., 1971).
The principal veins as well as smaller veins are green, the interveinal portion become chlorotic in Ailanthus triphysa (Anoop et al., 1998) followed by necrosis and browning of interveinal tissue in melons (Simon et al., 1986). The affected young leaves remain small and abscise before older leaves in birdsfoot trefoil (Russelle and McGraw, 1986).
The common symptoms of Mo deficiency in plants include a general yellowing, marginal and interveinal chlorosis, marginal necrosis, rolling, scorching and downward curling of margins in poinsettia cultivars (Cox and Bartley, 1987; Cox, 1992) and in various field, horticulture and forage crops (Gupta and Gupta, 1997). The deficiency of molybdenum in cauliflower causes the disorder described as ‘Whiptail’ ( Duval et al., 1991).
Plant growth is reduced and older leaves turn chlorotic giving plants a nitrogen deficient phenotype, when grown on urea-based nutrient solutions not supplemented with Ni in tomato and soybean (Shimada and Ando, 1980; Krogmeier et al., 1991). Similar results were obtained in oilseed-rape, zucchini and soybean by Gerendás and Sattelmacher (1997).
The characteristic deficiency symptom of nitrogen is the appearance of uniform yellowing of leaves including the veins, this being more pronounced on older leaves as expressed in rabbit-eye and blueberries (Tamada, 1989); Fescue (Razmjoo, 1997); Ailanthus triphysa (Anoop et al., 1998); chili (Balakrishnan 1999) and sugarcane (Nautiyal et al., 2000). The leaves become stiff and erect. In dicotyledonous crops the leaves detach easily under extreme deficiency condition. Cereal crops show characteristics ‘V’ shaped yellowing at the tip of lower leaves. O’Sullivan et al.,(1993) observed relatively small and pale green leaves with dull appearance in sweet potato. If such condition of nitrogen stress do persist, the result is a decreased foliage growth and shoot growth. See for example: black pepper (Nybe and Nair, 1986); douglas-fir (Friend et al.,1990) and sapota (Nachegowda et al.,1992).
In phosphorus deficiency, leaves remain small, erect, unusually dark green with greenish red in sweet potato (O’Sullivan et al., 1993), bluish green in chili (Balakrishnan 1999), brown in birdsfoot trefoil (Russelle and McGraw, 1986) or purplish tinge in sugar maple (Bernier and Brazeau, 1988); blueberry (Tamada,1989) and sugarcane (Nautiyal et al., 2000). The under side develops bronzy appearance. The root growth is also restricted under phosphorus stress in black pepper (Nybe and Nair, 1986). Anthocyanin pigment increases in leaves of barley (Hamy,1983) and Arabidopsis thaliana (Trull et al., 1997) under phosphorus stress,
Under potassium stress condition, yellowing of leaves starts from the tips or margins of leaves extending towards the center of leaf base. The yellowing is interveinal and irregular in the leaves of tomato (Besford, 1978) and blueberry (Tamada, 1989). These yellow parts become necrotic (dead spots) with leaf curling in tobacco (Arnold et al., 1986); sugar maple (Bernier and Brazeau, 1988); sapota (Nachegowda et al.,1992) and sugarcane (Nautiyal et al., 2000). There is a sharp difference between green, yellow and necrotic parts.
Sulfur deficiency cause leaves to become yellowish in black pepper (Nybe and Nair, 1987); potato (Gupta and Sanderson, 1993) and Brassica oleracea (Stuiver et al., 1997) and it appears similar to nitrogen deficiency, but the symptoms are first visible on younger leaves (Russelle and McGraw, 1986). The affected leaves are narrow and the veins are paler and chlorotic than interveinal portion, especially towards the base with marginal necrosis in sugarcane (Nautiyal et al., 2000).
The leaves become narrow and small in chili (Balakrishnan, 1999), the lamina becomes chlorotic in sweet potato (O’Sullivan et al., 1993), sour orange seedlings (Swietlik, 1995) and chickpea (Khan et al., 1998), while veins remain green. Subsequently, dead spots develop all over the leaf including veins, tips and margins under sever deficiency, shoot growth is reduced (O’Sullivan et al., 1993; Swietlik, 1995 and Yu and Rengel, 1999). Khaira disease in rice results due to zinc deficiency (Gautam and Sharma, 1982; Sharma et al., 1988 and Sahi et al., 1992). Shoot elongation is reduced and a tuft or rosette of distinctly narrow leaves is produced at the shoot terminal in apple and pear. The symptoms are termed ‘little leaf’ or ‘rosette’ (Hanson, 1993).
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