Factors Involved in Fruit Calcium Deficiency Disorders

Understanding the mechanisms of calcium (Ca2þ) deficiency disorder development in plants has been a challenge for more than a 100 years. Previous studies support the hypothesis that Ca2þ deficiency disorders can be triggered by mechanisms that reduce plant Ca2þ uptake from the soil, fruit Ca2þ uptake from the plant, and Ca2þ translocation within the fruit, and also result in abnormal regulation of cellular Ca2þ partitioning. Plant Ca2þ uptake can be determined by Ca2þ content and availability in the soil, root growth, activity of apoplastic and symplastic pathways of root Ca2þ uptake, as well as uptake competition between Ca2þ and other nutrients. Fruit Ca2þ uptake is determined by Ca2þ content in the xylem sap, and xylem/phloem ratio of fruit sap uptake, which is affected by the rates of leaf and fruit transpiration and growth. Calcium translocation to distal fruit tissue, containing the lowest fruit Ca2þ content and the highest susceptibility to Ca2þ deficiency disorders, is potentially dependent on the cell wall Ca2þ-binding capacity and symplastic Ca2þ uptake by the tissue at the peduncle end of the fruit, abundance of functional xylem vessels connecting peduncle and distal fruit tissues, as well as the hydrostatic gradient required for Ca2þ translocation towards the distal tissue. Cellular Ca2þ partitioning is defined by the activity of Ca2þ channels, Ca2þ ATPases, and Ca2þ exchangers present in cellular membranes, as well as the capacity of the cell wall to bind Ca2þ, and the formation of Ca2þ precipitates in different cellular compartments. Therefore, 107 Horticultural Reviews, Volume 40, First Edition. Edited by Jules Janick. 2012 Wiley-Blackwell. Published 2012 by John Wiley & Sons, Inc. Ca2þ deficiency disorders in fruit may not be caused by a single factor, but most likely by a combination of mechanisms that lower Ca2þ concentration at a specific tissue and cell localization, leading to Ca2þ deficiency symptoms.