Copper regulates primary root elongation through PIN1-mediated auxin redistribution.
Copper regulates primary root elongation through PIN1-mediated auxin redistribution.
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DOI：
10.1093/pcp/pct030
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发表时间：
2013-05
影响因子：
4.9
通讯作者：
Hong-mei Yuan;Heng-Hao Xu;Wen-Cheng Liu;Ying‐Tang Lu
中科院分区：
文献类型：
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作者：
Hong-mei Yuan;Heng-Hao Xu;Wen-Cheng Liu;Ying‐Tang Lu
重金属铜（Cu）是植物正常生长发育所必需的微量元素，但过量会抑制初生根的生长。过量铜在这一过程中的作用机制还有待进一步阐明。在这里，我们报道了高浓度的CuSO4通过影响伸长和分生组织区来抑制拟南芥幼苗的初生根伸长。在分生组织区，过量的铜降低了分生组织细胞的分裂电位。基于DR5::GUS表达谱的进一步实验表明，Cu可以调节生长素的分布，导致Cu处理根的伸长区和分生组织区生长素活性升高。这种cu介导的生长素再分配被证明是cu介导的初生根伸长抑制的原因。额外的遗传和生理数据表明，调节这一过程的是pinformmed1 (PIN1)，而不是PIN2或AUXIN1 （AUX1）。然而，cu诱导的过氧化氢积累并没有促进cu诱导的生长素重新分配，从而抑制根伸长。当分析乙烯在这一过程中的可能作用时，Cu对野生型和ein2-1突变体的根伸长都有相似的影响，这意味着Cu介导的对初生根伸长的抑制不是由于乙烯信号通路。
The heavy metal copper (Cu) is an essential microelement required for normal plant growth and development, but it inhibits primary root growth when in excess. The mechanism underlying how excess Cu functions in this process remains to be further elucidated. Here, we report that a higher concentration of CuSO4 inhibited primary root elongation of Arabidopsis seedlings by affecting both the elongation and meristem zones. In the meristem zone, meristematic cell division potential was reduced by excess Cu. Further experiments showed that Cu can modulate auxin distribution, resulting in higher auxin activities in both the elongation and meristem zones of Cu-treated roots based on DR5::GUS expression patterns. This Cu-mediated auxin redistribution was shown to be responsible for Cu-mediated inhibition of primary root elongation. Additional genetic and physiological data demonstrated that it was PINFORMED1 (PIN1), but not PIN2 or AUXIN1 (AUX1), that regulated this process. However, Cu-induced hydrogen peroxide accumulation did not contribute to Cu-induced auxin redistribution for inhibition of root elongation. When the possible role of ethylene in this process was analyzed, Cu had a similar impact on the root elongation of both the wild type and the ein2-1 mutant, implying that Cu-mediated inhibition of primary root elongation was not due to the ethylene signaling pathway.