氯化鈣噴施與高磷養液對番茄尻腐病發生率及細胞內鈣離子分布之影響

Abstract

番茄尻腐病(blossom-end rot)為影響果實外觀及產量的生理障礙(physiological disorder)。多數研究認為果實果臍端(blossom-end)缺鈣為尻腐病發生的主要生理原因，然而後來的研究發現尻腐病果實具有與健康果實相似的總鈣濃度。近年有學者提出細胞中鈣離子體內失衡可能為尻腐病發生原因之假說。葉面及果實施鈣為農民常使用之防治方法，提高水耕養液中鈣和磷濃度也被證實能減緩尻腐病發生率，但鈣和磷彼此間對尻腐病的交互作用機制尚未被闡明。本研究使用對尻腐病敏感之大果番茄‘Heinz 1706’進行試驗，先前研究多是以水耕番茄進行鈣、磷濃度相關試驗，然臺灣農民多以土壤或無土介質栽培番茄。因此本研究採用介質耕方式搭配肥液滴灌系統進行，使用不同防治方法，探討其對番茄果實外觀、尻腐病發生率及嚴重度、營養元素濃度、細胞鈣離子濃度及分布之影響。試驗一處理為果實噴施0.5%氯化鈣水溶液與否，結果顯示，噴施0.5%氯化鈣水溶液果實呈現較低的果長、果寬、單果重、尻腐病發生率及嚴重度、細胞膜滲漏度，同時具有較高的總鈣含量、質外體鈣離子濃度(apoplastic Ca2+ concentration, [Ca2+]apoplast)及細胞質液鈣離子濃度(cytosolic Ca2+ concentration, [Ca2+]cyt)，以及大量鈣離子沈澱於細胞膜與細胞壁間。以授粉後45天果實而言，對照組與處理組之無發病果實較尻腐病果實具有較高之細胞質液鈣離子濃度，以及較多鈣離子沈澱於細胞膜與細胞壁間。試驗二為調控養液中磷濃度與鹽濃度。磷濃度不影響果實外觀、尻腐病發生率及嚴重度；與於中磷濃度養液中生長的果實相比，高磷處理僅在紅熟果顯示出較高的總鈣濃度；不同磷濃度處理並不顯著影響質外體鈣離子濃度，但高磷處理細胞質液鈣離子濃度高於中磷處理。相較無鹽處理，高鹽果實較小且有較高尻腐病發生率及嚴重度；不同鹽度處理對質外體鈣離子濃度與細胞質液鈣離子濃度無顯著影響。上述結果顯示噴施0.5%氯化鈣水溶液處理能有效降低尻腐病發生，磷養液處理效果則不明顯，因此防治尻腐病仍應以噴施0.5%氯化鈣水溶液效用較佳。尻腐病果實具有較低質外體鈣離子濃度、細胞質液鈣離子濃度與細胞層級鈣離子分布，支持了細胞中鈣離子體內失衡可能誘發尻腐病的假說。

Tomato blossom-end rot (BER) is a physiological disorder which affects fruit appearance and yield. In most studies, calcium deficiency in distal part of fruit is considered to be the major physiological cause of BER. However, fruits with BER are found to have similar total calcium concentration to healthy fruits in later researches. Recently, researchers proposed a hypothesis that the imbalance of calcium ion (Ca2+) homeostasis in cell could trigger BER. Farmers spray calcium on leaves and fruits as a common prevention of BER. Increasing calcium and phosphorus concentration in nutrient solution is also proved to alleviate BER incidence. However, the interactive effect between calcium and phosphorus to BER has not been elucidated. In this research, BER-sensitive tomato cultivar ‘Heinz 1706’ were used as the material. Most previous studies related to BER were undertaken by hydroponic culture, while most tomatoes in Taiwan are cultivated by soil or soilless substrate. Therefore, this research used substrate culture with trickle fertigation system to investigate the effects of different preventions on tomato fruit appearance, BER incidence, BER severity, concentration of mineral elements, and cellular calcium concentration and distribution. In experiment I, fruits were sprayed with/without 0.5% calcium chloride (CaCl2) solution. The results showed that fruit sprayed with 0.5% CaCl2 solution displayed smaller length, width, and single fruit weight, along with lower incidence and severity of BER, and electrolyte leakage. In the mean time they had higher total calcium concentration, fruit apoplastic calcium concentration ([Ca2+]apoplast), cytosolic calcium concentration ([Ca2+]cyt), and abundant Ca2+ precipitated between cell membrane and cell wall. In the case of fruit 45 days after pollination (DAP), the healthy fruits of the control group and the treated group had higher [Ca2+]cyt than the BER fruits, and more Ca2+ precipitated between cell membrane and cell wall. Adjusting phosphorus concentration and salinity in nutrient solution were carried out in experiment II. Phosphorus concentration had no effect on fruit appearance, BER incidence and severity. Compared to fruits grown in nutrient solution with medium phosphorus concentration, the ones treated with high phosphorus concentration showed higher total calcium concentration only during red stage. Different phosphorus concentrations treatment did not significantly affect [Ca2+]apoplast. But high phosphorus treatment had higher [Ca2+]cyt than medium phosphorus treatment. High salinity treated fruits showed smaller size, higher BER incidence and severity than the ones without salinity treatment. Different salinity treatment did not significantly affect [Ca2+]apoplast and [Ca2+]cyt. The above results indicate that spraying 0.5% CaCl2 solution effectively decreases BER incidence, while the effect of high phosphorus in nutrient solution is not obvious. Therefore, spraying 0.5% CaCl2 solution is a better treatment to prevent BER. Fruits with BER have lower [Ca2+]apo, [Ca2+]cyt and cellular Ca2+ distribution, which supports the hypothesis that BER could be triggered by the imbalance of Ca2+ homeostasis in cell.