Expression of a moderately anionic peroxidase is induced by aluminum treatment in tobacco cells: Possible involvement of peroxidase isozymes in aluminum ion stress
Expression of a moderately anionic peroxidase is induced by aluminum treatment in tobacco cells: Possible involvement of peroxidase isozymes in aluminum ion stress
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DOI：
10.1111/j.1399-3054.1996.tb00178.x
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发表时间：
1996-01-01
影响因子：
6.4
通讯作者：
Matsumoto, H
中科院分区：
文献类型：
--
作者：
Ezaki, B;Tsugita, S;Matsumoto, H
为了阐明铝毒和耐铝机制，我们从烟草cDNA文库中克隆了一个新的基因克隆pAL 201。北方杂交分析表明，铝处理和磷（P-1）饥饿诱导了pAL 201的表达。完整的cDNA序列表明，该克隆编码中度阴离子过氧化物酶（EC 1.11.1.7）。等电聚焦分析表明，中度阴离子过氧化物酶（约pI6.7）和两个阳离子过氧化物酶（pI9.2和9.7）的可溶性部分被激活铝处理和P-1饥饿，而两个中度阴离子同工酶被这些压力抑制。我们推测铝离子胁迫可以控制某些过氧化物酶同工酶的活性，其中之一可能是由pAL 201基因表达增强引起的。这些同工酶可能在铝离子胁迫中起一定的作用。
To clarify the mechanism of aluminum (Al) toxicity and Al tolerance, we isolated a new clone (pAL201) from a tobacco cDNA library. Northern blot hybridization analysis indicated that the expression of pAL201 is induced by Al treatment and phosphate (P-i) starvation. The complete cDNA sequence suggested that this clone encodes a moderately anionic peroxidase (EC 1.11.1.7). Analysis by isoelectric focussing indicated that a moderately anionic peroxidase (approximately pI 6.7) and two cationic peroxidases (pI 9.2 and 9.7) in the soluble fraction are activated by Al treatment and P-i starvation, while two moderately anionic isozymes are repressed by these stresses. We suppose that Al ion stress can control the activity of some peroxidase isozymes, one of which is probably induced by enhanced gene expression of pAL201. There is a possibility that some of these isozymes have some functions in Al ion stress.