A Mutant Strain Arabidopsis thaliana that Lacks Vacuolar Membrane Zinc Transporter MTP1 Revealed the Latent Tolerance to Excessive Zinc

A Mutant Strain Arabidopsis thaliana that Lacks Vacuolar Membrane Zinc Transporter MTP1 Revealed the Latent Tolerance to Excessive Zinc
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DOI:
10.1093/pcp/pcp067
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发表时间:
2009-06-01
影响因子:
4.9
通讯作者:
Maeshima, Masayoshi
Maeshima, Masayoshi
中科院分区:
生物学2区
文献类型:
--
作者:
Kawachi, Miki;Kobae, Yoshihiro;Maeshima, Masayoshi

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一个缺乏液泡膜锌-2/H逆向转运蛋白MTP1的拟南芥突变系对锌敏感。我们研究了这个功能丧失的突变体在高锌条件下的生理变化,以了解其对锌胁迫的适应机制。通过X射线能谱分析发现,在过量锌胁迫下,野生型根在液泡状细胞器中积累锌,而突变体根不积累锌。化学分析表明,突变根的含锌量仅为高锌条件下野生根的1/3。在500M硫酸锌溶液中,mtp1-1幼苗的根系生长受到严重抑制。过量锌对细胞分裂和伸长的抑制是可逆的,细胞在正常培养液中恢复生长。在突变根中,在MTP1基因高表达的分生区出现了明显的ROS形成。锌处理增强了与锌耐性有关的几个基因的表达:质膜锌-2输出ATPase、HMA4、质膜和液泡膜质子泵。参与ROS解毒的CuZn-超氧化物歧化酶也被诱导。细胞质膜锌摄取转运蛋白ZIP1的表达受到抑制。这些基因的上调或下调可能使植物对锌毒害产生抗性。这些结果表明MTP1在过量锌的解毒中起着重要作用,并为MTP1隐藏的对锌胁迫的潜在适应机制提供了新的信息。
A mutant line of Arabidopsis thaliana that lacks a vacuolar membrane Zn-2/H antiporter MTP1 is sensitive to zinc. We examined the physiological changes in this loss-of-function mutant under high-Zn conditions to gain an understanding of the mechanism of adaptation to Zn stress. When grown in excessive Zn and observed using energy-dispersive X-ray analysis, wild-type roots were found to accumulate Zn in vacuolar-like organelles but mutant roots did not. The Zn content of mutant roots, determined by chemical analysis, was one-third that of wild-type roots grown in high-Zn medium. Severe inhibition of root growth was observed in mtp1-1 seedlings in 500M ZnSO4. Suppression of cell division and elonga-tion by excessive Zn was reversible and the cells resumed growth in normal medium. In mutant roots, a marked formation of reactive oxygen species (ROS) appeared in the meristematic zone, where the MTP1 gene was highly expressed. Zn treatment enhanced the expression of several genes involved in Zn tolerance: namely, the plasma membrane Zn-2-export ATPase, HMA4, and plasma and vacuolar membrane proton pumps. CuZn-superoxide dismutases, involved in the detoxification of ROS, were also induced. The expression of plasma membrane Zn-uptake transporter, ZIP1, was suppressed. The up- or down-regulation of these genes might confer the resistance to Zn toxicity. These results indicate an essential role of MTP1 in detoxification of excessive Zn and provide novel information on the latent adaptation mechanism to Zn stress, which is hidden by MTP1.