Mutations in an Atypical TIR-NB-LRR-LIM Resistance Protein Confer Autoimmunity.
Mutations in an Atypical TIR-NB-LRR-LIM Resistance Protein Confer Autoimmunity.
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DOI：
10.3389/fpls.2011.00071
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发表时间：
2011
影响因子：
5.6
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
Bi D;Johnson KC;Zhu Z;Huang Y;Chen F;Zhang Y;Li X
为了抵御微生物感染，植物采用了一个复杂的免疫系统，该系统部分依赖于抗性(R)蛋白，在病原体检测时启动复杂的信号级联反应。植物利用的抗性信号网络只被部分描述。通过基因筛选来鉴定参与该网络的新型防御调节因子，分离出snc6-1D突变体。定位克隆发现该突变体在冷敏感3 （CHS3）基因中含有一个分子损伤，因此该等位基因被重新命名为CHS3 - 2d。CHS3编码一个含有c端锌结合LIM （Lin-11, il -1, Mec-3）结构域的TIR-NB-LRR R蛋白。虽然该蛋白先前与冷应激和防御反应有关，但LIM结构域在调节蛋白质活性中的作用尚不清楚。chv3 - 2d等位基因包含一个G到a点突变，导致靠近LIM结构域的C1340到Y1340的替换。它编码了一个显性的功能获得突变。chs3-2D突变体发育严重，叶片卷曲。此外，它还组成性地表达致病相关（PR）基因，积累水杨酸，并对强毒卵菌分离物拟南芥透明operonospora拟南芥（h.a.）表现出增强的抗性。Noco2。使用GFP融合构建的亚细胞定位分析表明，CHS3和CHS3 - 2d都定位于细胞核。第三个chs3突变等位基因chs3- 3d，在我们实验室的一个不相关的遗传筛选中被鉴定出来。该等位基因包含一个C到T点突变，导致LRR-LIM连接区域的M1017到V1017替换。此外，chs3-2D抑制基因筛选发现了两个包含二级突变的反向等位基因，这些突变基因消除了突变体的形态。对这些分子损伤位置的分析为LIM结构域抑制CHS3 r样蛋白活性的假设提供了支持。这种抑制可能通过自身抑制或结合负防御调节因子发生。
In order to defend against microbial infection, plants employ a complex immune system that relies partly on resistance (R) proteins that initiate intricate signaling cascades upon pathogen detection. The resistance signaling network utilized by plants is only partially characterized. A genetic screen conducted to identify novel defense regulators involved in this network resulted in the isolation of the snc6-1D mutant. Positional cloning revealed that this mutant contained a molecular lesion in the chilling sensitive 3 (CHS3) gene, thus the allele was renamed chs3-2D. CHS3 encodes a TIR-NB-LRR R protein that contains a C-terminal zinc-binding LIM (Lin-11, Isl-1, Mec-3) domain. Although this protein has been previously implicated in cold stress and defense response, the role of the LIM domain in modulating protein activity is unclear. The chs3-2D allele contains a G to A point mutation causing a C1340 to Y1340 substitution close to the LIM domain. It encodes a dominant gain-of-function mutation. The chs3-2D mutant is severely stunted and displays curled leaf morphology. Additionally, it constitutively expresses PATHOGENESIS-RELATED (PR) genes, accumulates salicylic acid, and shows enhanced resistance to the virulent oomycete isolate Hyaloperonospora arabidopsidis (H.a.) Noco2. Subcellular localization assays using GFP fusion constructs indicate that both CHS3 and chs3-2D localize to the nucleus. A third chs3 mutant allele, chs3-3D, was identified in an unrelated genetic screen in our lab. This allele contains a C to T point mutation resulting in an M1017 to V1017 substitution in the LRR–LIM linker region. Additionally, a chs3-2D suppressor screen identified two revertant alleles containing secondary mutations that abolish the mutant morphology. Analysis of the locations of these molecular lesions provides support for the hypothesis that the LIM domain represses CHS3 R-like protein activity. This repression may occur through either autoinhibition or binding of a negative defense regulator.
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