The Vacuolar Manganese Transporter MTP8 Determines Tolerance to Iron Deficiency-Induced Chlorosis in Arabidopsis
The Vacuolar Manganese Transporter MTP8 Determines Tolerance to Iron Deficiency-Induced Chlorosis in Arabidopsis
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DOI：
10.1104/pp.15.01194
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发表时间：
2016-02-01
期刊：
影响因子：
7.4
通讯作者：
Peiter, Edgar
中科院分区：
文献类型：
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作者：
Eroglu, Seckin;Meier, Bastian;Peiter, Edgar
铁（Fe）缺乏是石灰性土壤上一种广泛存在的营养失调症。为了鉴定参与铁缺乏响应的基因，在铁有效性低的高pH培养基上对拟南芥（Arabidopsis thaliana）T-DNA插入系进行了筛选。这种方法鉴定出金属耐受蛋白8（MTP8），它是阳离子扩散促进因子家族的一个成员，是耐受铁缺乏诱导的黄化的关键决定因素，在土壤基质中也是如此。亚细胞定位到液泡膜、对锰（Mn）敏感的酿酒酵母菌株的互补以及mtp8敲除突变体对锰的敏感性，都表明该蛋白是一种液泡锰转运蛋白，可防止植物细胞遭受锰毒害。MTP8的表达在低铁以及高锰培养基上都被强烈诱导，这两者都严格依赖于转录因子FIT，表明高锰胁迫会诱导铁缺乏。当培养基中存在锰时，mtp8突变体仅对铁缺乏高度敏感，这进一步表明在铁限制期间MTP8具有特定于锰的作用。在这些条件下，mtp8突变体不仅向地上部分转运的锰比野生型植物多，而且尤其遭受极低的铁浓度，因此出现铁黄化，尽管mtp8中对铁缺乏的转录响应被更强烈地上调。mtp8突变体从含锰的低铁培养基中吸收铁的能力下降是由于其提高铁螯合物还原酶活性的能力受损，而铁螯合物还原酶活性是铁获取的一个关键过程。这些发现为长期以来已知的锰对铁营养的干扰提供了一种机制解释，并确定了植物缓解这种拮抗作用的分子过程。
Iron (Fe) deficiency is a widespread nutritional disorder on calcareous soils. To identify genes involved in the Fe deficiency response, Arabidopsis (Arabidopsis thaliana) transfer DNA insertion lines were screened on a high-pH medium with low Fe availability. This approach identified METAL TOLERANCE PROTEIN8 (MTP8), a member of the Cation Diffusion Facilitator family, as a critical determinant for the tolerance to Fe deficiency-induced chlorosis, also on soil substrate. Subcellular localization to the tonoplast, complementation of a manganese (Mn)-sensitive Saccharomyces cerevisiae yeast strain, and Mn sensitivity of mtp8 knockout mutants characterized the protein as a vacuolar Mn transporter suitable to prevent plant cells from Mn toxicity. MTP8 expression was strongly induced on low-Fe as well as high-Mn medium, which were both strictly dependent on the transcription factor FIT, indicating that high-Mn stress induces Fe deficiency. mtp8 mutants were only hypersensitive to Fe deficiency when Mn was present in the medium, which further suggested an Mn-specific role of MTP8 during Fe limitation. Under those conditions, mtp8 mutants not only translocated more Mn to the shoot than did wild-type plants but suffered in particular from critically low Fe concentrations and, hence, Fe chlorosis, although the transcriptional Fe deficiency response was up-regulated more strongly in mtp8. The diminished uptake of Fe from Mn-containing low-Fe medium by mtp8 mutants was caused by an impaired ability to boost the ferric chelate reductase activity, which is an essential process in Fe acquisition. These findings provide a mechanistic explanation for the long-known interference of Mn in Fe nutrition and define the molecular processes by which plants alleviate this antagonism.