FATTY ACID DESATURASE5 Is Required to Induce Autoimmune Responses in Gigantic Chloroplast Mutants of Arabidopsis
FATTY ACID DESATURASE5 Is Required to Induce Autoimmune Responses in Gigantic Chloroplast Mutants of Arabidopsis
复制标题
拟南芥巨型叶绿体突变体需要脂肪酸去饱和酶5诱导自身免疫反应
DOI：
10.1105/tpc.20.00016
复制
发表时间：
2020-10-01
期刊：
影响因子：
11.6
通讯作者：
Kim, Chanhong
中科院分区：
文献类型：
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作者：
Li, Bingqi;Fang, Jun;Kim, Chanhong
遗传损伤的质体分裂导致活性氧和脂质过氧化的爆发，引起自身免疫反应的激活。叶绿体通过叶绿体到核的逆行信号传导介导遗传控制的细胞死亡。为了解释这一机制，我们研究了叶绿体连接的损伤模拟突变体的拟南芥（拟南芥）缺乏质体分裂，从而发展巨大的叶绿体（GC）。这些GC突变体，包括皱叶（crl），组成性表达免疫相关基因，并显示光依赖性局部细胞死亡（LCD），反映了典型的自身免疫反应。我们的反向遗传方法排除了免疫/应激激素在触发LCD中的任何潜在作用。相反，转录组和计算机模拟分析表明，通过多不饱和脂肪酸（PUFA）氧化或脂质过氧化驱动的信号传导产生的反应性亲电物质（RES）可能会诱导LCD。与这些结果一致，crl的抑制子之一，被称为spcrl 4，在编码叶绿体定位的脂肪酸脱饱和酶5（FAD 5）的核基因中包含一个致病突变，该突变催化棕榈酸（16：0）转化为棕榈油酸（16：1）。在crl突变体中FAD 5的损失可能会减弱RES和/或脂质过氧化的水平，这是由于棕榈酸驱动的PUFA的水平降低，PUFA是活性氧的主要目标。fad 5还损害免疫相关基因的表达和其他GC突变体中LCD的发展的事实证实了内在逆行信号传导途径的存在，以FAD 5依赖性方式引发自身免疫应答。
Genetically impaired plastid division leads to a burst of reactive oxygen species and lipid peroxidation, causing the activation of autoimmune responses.Chloroplasts mediate genetically controlled cell death via chloroplast-to-nucleus retrograde signaling. To decipher the mechanism, we examined chloroplast-linked lesion-mimic mutants of Arabidopsis (Arabidopsis thaliana) deficient in plastid division, thereby developing gigantic chloroplasts (GCs). These GC mutants, including crumpled leaf (crl), constitutively express immune-related genes and show light-dependent localized cell death (LCD), mirroring typical autoimmune responses. Our reverse genetic approach excludes any potential role of immune/stress hormones in triggering LCD. Instead, transcriptome and in silico analyses suggest that reactive electrophile species (RES) generated via oxidation of polyunsaturated fatty acids (PUFAs) or lipid peroxidation-driven signaling may induce LCD. Consistent with these results, the one of the suppressors of crl, dubbed spcrl4, contains a causative mutation in the nuclear gene encoding chloroplast-localized FATTY ACID DESATURASE5 (FAD5) that catalyzes the conversion of palmitic acid (16:0) to palmitoleic acid (16:1). The loss of FAD5 in the crl mutant might attenuate the levels of RES and/or lipid peroxidation due to the reduced levels of palmitic acid-driven PUFAs, which are prime targets of reactive oxygen species. The fact that fad5 also compromises the expression of immune-related genes and the development of LCD in other GC mutants substantiates the presence of an intrinsic retrograde signaling pathway, priming the autoimmune responses in a FAD5-dependent manner.