The root cell wall is the first and primary target of aluminum (Al) toxicity. Monocots such as rice (Oryza sativa) can accumulate appreciable levels of hydroxycinnamic acids (HCAs) to modify and cross‐link hemicellulose and/or lignin of the cell wall. Nevertheless, it is unclear whether this HCA‐mediated modification of the cell wall is important for Al accumulation and resistance. We previously isolated and characterized a rice ral1 (resistance to aluminum 1) mutant that shows enhanced Al resistance. In this study, we cloned RAL1 and found that it encodes the 4‐coumarate:coenzyme A ligase 4CL4, an enzyme putatively involved in lignin biosynthesis. Mutation of RAL1/4CL4 reduces lignin content and increases the accumulation of its substrates 4‐coumaric acid (PA) and ferulic acid (FA). We demonstrate that altered lignin accumulation is not required for the enhanced Al resistance in ral1/4cl4 mutants. We found that the increased accumulation of PA and FA can reduce Al binding to hemicellulose and consequently enhance Al resistance in ral1/4cl4 mutants. Al stress is able to trigger PA and FA accumulation, which is likely caused by the repression of the expression of RAL1/4CL4 and its homologous genes. Our results thus reveal that Al‐induced PA and FA accumulation is actively and positively involved in Al resistance in rice through the modification of the cell wall and thereby the reduced Al binding to the cell wall.

中文翻译：

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4-香豆酸酯：辅酶A连接酶4CL4的功能障碍影响水稻的铝抗性和木质素积累

根细胞壁是铝（Al）毒性的首要目标。单子叶植物，例如水稻（Oryza sativa）可以积累一定水平的羟基肉桂酸（HCA），以修饰和交联细胞壁的半纤维素和/或木质素。然而，尚不清楚这种HCA介导的细胞壁修饰是否对Al的积累和抗性重要。我们以前分离并表征稻RAL1（ř esistance到人uminum 1）突变体显示增强的铝的电阻。在这项研究中，我们克隆了RAL1，发现它编码4香豆酸酯：辅酶A连接酶4CL4，这是一种推测参与木质素生物合成的酶。RAL1突变/ 4CL4减少了木质素含量，并增加了其底物4-香豆酸（PA）和阿魏酸（FA）的积累。我们证明，改变的木质素积累不是必需的ral1 / 4cl4突变体中增强的Al抗性。我们发现，PA和FA积累的增加可以减少Al与半纤维素的结合，从而增强ral1 / 4cl4突变体对Al的抗性。Al胁迫能够触发PA和FA积累，这很可能是由于RAL1 / 4CL4表达的抑制所致及其同源基因。因此，我们的结果表明，铝诱导的PA和FA积累通过修饰细胞壁，从而减少了铝与细胞壁的结合，积极而积极地参与了水稻对铝的抗性。