Polyamine biosynthesis of apple callus under salt stress: importance of the arginine decarboxylase pathway in stress response
Polyamine biosynthesis of apple callus under salt stress: importance of the arginine decarboxylase pathway in stress response
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DOI：
10.1093/jxb/erl018
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发表时间：
2006-08-01
影响因子：
6.9
通讯作者：
Moriguchi, Takaya
中科院分区：
文献类型：
--
作者：
Liu, Ji-Hong;Nada, Kazuyoshi;Moriguchi, Takaya
为了阐明精氨酸脱羧酶（ADC）途径在盐胁迫反应中的作用，以苹果[Malus sylvestris（L.）Mill.变种Artistica（Borkh.）Mansf.]在盐胁迫下、胁迫后恢复期以及ADC抑制剂D-精氨酸抑制ADC时，对离体愈伤组织进行了形态学观察。盐胁迫（200 mM NaCl）引起的硫代巴比妥酸反应物质（TBARS）和电解质渗漏（EL）的愈伤组织，这是伴随着游离腐胺含量的增加，在7天的治疗。结合腐胺也有所增加，但这种增加仅限于盐胁迫初期。腐胺的积累与ADC活性的诱导和苹果ADC基因（MdADC）的表达一致。当用200 mM NaCl处理过的愈伤组织转移到含有（连续胁迫）或不含（恢复）NaCl的新鲜培养基中时，与连续胁迫处理相比，TBARS和EL在恢复处理中显著降低，表明促进了新愈伤组织细胞的形成。同时，恢复期愈伤组织中MdADC的表达和ADC的活性均降低，而连续胁迫下愈伤组织中MdADC的表达和活性均升高。鸟氨酸脱羧酶（ODC）的活性表现出相反的模式ADC在这些条件下。在盐胁迫下，D-精氨酸处理比不处理导致更严重的生长障碍。此外，D-精氨酸处理的愈伤组织中腐胺的积累、MdADC的诱导和ADC的激活与未处理的愈伤组织不具有可比性。外源腐胺的添加可以缓解盐胁迫，表现为鲜重增加和EL值增加。所有这些结果表明，ADC途径密切参与盐胁迫反应。腐胺在盐胁迫下的积累，腐胺在减轻胁迫损害中可能的生理作用，以及MdADC和ADC在盐胁迫响应中的参与进行了讨论。
To clarify the involvement of the arginine decarboxylase (ADC) pathway in the salt stress response, the polyamine titre, putrescine biosynthetic gene expression, and enzyme activities were investigated in apple [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.] in vitro callus under salt stress, during recovery after stress, and when ADC was inhibited by D-arginine, an inhibitor of ADC. Salt stress (200 mM NaCl) caused an increase in thiobarbituric acid-reactive substances (TBARS) and electrolyte leakage (EL) of the callus, which was accompanied by an increase in free putrescine content, during 7 d of treatment. Conjugated putrescine was also increased, but this increase was limited to the early stage of salt stress. Accumulation of putrescine was in accordance with induction of ADC activity and expression of the apple ADC gene (MdADC). When callus that had been treated with 200 mM NaCl was transferred to fresh medium with (successive stress) or without (recovery) NaCl, TBARS and EL were significantly reduced in the recovery treatment, indicating promotion of formation of new callus cells, compared with the successive stress treatment. Meanwhile, MdADC expression and ADC activity were also decreased in the callus undergoing recovery, whereas those of the callus under successive stress were increased. Ornithine decarboxylase (ODC) activity showed a pattern opposite to that of ADC in these conditions. D-Arginine treatment led to more serious growth impairment than no treatment under salt stress. In addition, accumulation of putrescine, induction of MdADC, and activation of ADC in D-arginine-treated callus were not comparable with those of the untreated callus. Exogenous addition of putrescine could alleviate salt stress in terms of fresh weight increase and EL. All of these findings indicated that the ADC pathway was tightly involved in the salt stress response. Accumulation of putrescine under salt stress, the possible physiological role of putrescine in alleviating stress damage, and involvement of MdADC and ADC in response to salt stress are discussed.