The Arabidopsis stearoyl-acyl carrier protein-desaturase family and the contribution of leaf isoforms to oleic acid synthesis
The Arabidopsis stearoyl-acyl carrier protein-desaturase family and the contribution of leaf isoforms to oleic acid synthesis
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DOI：
10.1007/s11103-006-9086-y
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发表时间：
2007-01-01
影响因子：
5.1
通讯作者：
Kachroo, Pradeep
中科院分区：
文献类型：
--
作者：
Kachroo, Aardra;Shanklin, John;Kachroo, Pradeep
在植物中，油酸（18：1），一种主要的单不饱和脂肪酸（FA）的水平的变化，导致水杨酸（SA）和茉莉酸（JA）介导的防御反应的改变。这在拟南芥ssi 2/fab 2突变体中是明显的，其编码缺陷的硬脂酰-酰基载体蛋白-去饱和酶（S-ACP-DES），因此积累高水平的硬脂酸（18：0）和低水平的18：1。除了SSI 2，拟南芥基因组编码6个S-ACP-DES样酶，其天然表达水平不能补偿SSI 2中的功能丧失突变。在fab 2无效突变体中存在低水平的18：1表明一种或多种S-ACP-DES同工酶对18：1库有贡献。生化分析表明，除了SSI 2，其他四种同工酶能够去饱和18：0-ACP，但具有大大降低的比活性，这可能解释了这些SSI 2同工酶不能取代缺陷SSI 2。在S-ACP-DES 1和S-ACP-DES 4中含有T-DNA插入的品系显示它们的脂质谱发生了改变，但含有正常的18：1水平。然而，S-ACP-DES 1亚型在Ssi 2植物中的过表达导致18：1水平的恢复，从而挽救了所有Ssi 2相关的表型。因此，需要低比活性S-ACP-DES的高表达来补偿ssi 2中的突变。S-ACP-DES同种型的转录水平在高18：1含量的植物中降低。去饱和酶同工型在5倍过量的18：1-ACP中的酶活性显示出高达73%的产物抑制。这些数据共同表明，18：1水平在转录和翻译后水平上都受到调节。
In plants, changes in the levels of oleic acid (18:1), a major monounsaturated fatty acid (FA), results in the alteration of salicylic acid (SA)- and jasmonic acid (JA)-mediated defense responses. This is evident in the Arabidopsis ssi2/fab2 mutant, which encodes a defective stearoyl-acyl carrier protein-desaturase (S-ACP-DES) and consequently accumulates high levels of stearic acid (18:0) and low levels of 18:1. In addition to SSI2, the Arabidopsis genome encodes six S-ACP-DES-like enzymes, the native expression levels of which are unable to compensate for a loss-of-function mutation in ssi2. The presence of low levels of 18:1 in the fab2 null mutant indicates that one or more S-ACP-DES isozymes contribute to the 18:1 pool. Biochemical assays show that in addition to SSI2, four other isozymes are capable of desaturating 18:0-ACP but with greatly reduced specific activities, which likely explains the inability of these SSI2 isozymes to substitute for a defective ssi2. Lines containing T-DNA insertions in S-ACP-DES1 and S-ACP-DES4 show that they are altered in their lipid profile but contain normal 18:1 levels. However, overexpression of the S-ACP-DES1 isoform in ssi2 plants results in restoration of 18:1 levels and thereby rescues all ssi2-associated phenotypes. Thus, high expression of a low specific activity S-ACP-DES is required to compensate for a mutation in ssi2. Transcript level of S-ACP-DES isoforms is reduced in high 18:1-containing plants. Enzyme activities of the desaturase isoforms in a 5-fold excess of 18:1-ACP show product inhibition of up to 73%. Together these data indicate that 18:1 levels are regulated at both transcriptional and post-translational levels.