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Plant Nutrition » Macronutrients » Potassium

Symptoms of Deficiency

Content

⇒ Historical Information
⇒ Determination of Essentiality
  ⇒ Function in Plants
    - Enzyme Activation
    - Protein Synthesis
    - Ion Absorption and Transport
      » Potassium Absorption
      » Potassium Transport within Tissues
      » Osmotic Function
    - Photosynthesis and Respiration
    - Long-Distance Transport
⇒ Diagnosis of Potassium Status in Plants
  ⇒ Symptoms of Deficiency
  ⇒ Symptoms of Excess
⇒ Concentrations of Potassium in Plants
⇒ Assessment of Potassium Status in Soils
  ⇒ Potassium-Bearing Minerals
  ⇒ Potassium Fractions in Soils
  ⇒ Plant-Available Potassium
  ⇒ Soil Tests for Potassium Fertilizer Recommendations
⇒ Potassium Fertilizers
  ⇒ Kinds of Fertilizers
  ⇒ Application of Potassium Fertilizers
⇒ References
 

The beginning of K+ deficiency in plants is growth retardation, which is a rather nonspecific symptom and is thus not easily recognized as K+ deficiency. The growth rate of internodes is affected (51), and some dicotyledonous species may form rosettes (52). With the advance of K+ deficiency, old leaves show the first symptoms as under such conditions K+ is translocated from older to younger leaves and growing tips via the phloem. In most plant species, the older leaves show chlorotic and necrotic symptoms as small stripes along the leaf margins, beginning at the tips and enlarging along leaf margins in the basal direction. This type of symptom is particularly typical for monocotyledonous species.


The leaf margins are especially low in K+, and for this reason, they lose turgor, and the leaves appear flaccid. This symptom is particularly obvious in cases of a critical water supply. In some plant species, e.g., white clover (Trifolium repens L.), white and necrotic spots appear in the intercostal areas of mature leaves, and frequently, these areas are curved in an upward direction. Such symptoms result from a shrinkage and death of cells (53) because of an insufficient turgor. Growth and differentiation of xylem and phloem tissue is hampered more than the growth of the cortex. Thus, the stability and elasticity of stems is reduced so that plants are more prone to lodging (54). In tomato (Lycopersicon esculentum Mill.) fruits insufficiently supplied with K+, maturation is disturbed, and the tissue around the fruit stem remains hard and green (55). The symptom is called greenback and it has a severe negative impact on the quality of tomato.

At an advanced stage of K+ deficiency, chloroplasts (56) and mitochondria collapse (57). Potassium-deficient plants have a low-energy status (58) because, as shown above, K+ is essential for efficient energy transfer in chloroplasts and mitochondria. This deficiency has an impact on numerous synthetic processes, such as synthesis of sugar and starch, lipids, and ascorbate (59) and also on the formation of leaf cuticles. The latter are poorly developed under K+ deficiency (15). Cuticles protect plants against water loss and infection by fungi. This poor development of cuticles is one reason why plants suffering from insufficient K+ have a high water demand and a poor water use efficiency (WUE, grams of fresh beet root matter per grams of water consumed).

Sugar beet grown with insufficient K+, and therefore showing typical K+ deficiency, had a WUE of 5.5. Beet plants with a better, but not yet optimum, K+ supply, and showing no visible K+ deficiency symptoms, had a WUE of 13.1, and beet plants sufficiently supplied with K+ had a WUE of 15.4 (60). Analogous results were found for wheat (Triticum aestivum L.) grown in solution culture (61). The beneficial effect of K+ on reducing fungal infection has been observed by various authors (54,61,62). The water-economizing effect of K+ and its protective efficiency against fungal infection are of great ecological relevance.


Severe K+ deficiency leads to the synthesis of toxic amines such as putrescine and agmatine; in the reaction sequence arginine is the precursor (63). The synthetic pathway is induced by a low cytosolic pH, which presumably results from insufficient pumping of H+ out of the cell by the plasmalemma H+-ATPase, which requires K+ for full activity. The reaction sequence is as follows:
• Arginine is decarboxylated to agmatine
• Agmatine is deaminated to carbamylputrescine
• Carbamylputrescine is hydrolyzed into putrescine and carbamic acid

 

 

 

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