Background

Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood.

Results

Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3–5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H₂O₂ in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212.

Conclusion

These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

中文翻译：

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OsPG1编码一种聚半乳糖醛酸酶，该酶决定了细胞壁的结构并影响水稻对白叶枯病病原菌的抗性

背景

植物细胞壁是病原体定植在植物组织中的主要物理屏障。细胞壁完整性（CWI）的改变可通过破坏参与细胞壁生物合成，降解和重塑或由于生物或非生物胁迫引起的细胞壁破坏的蛋白质来激活特定防御。聚半乳糖醛酸酶（PG）通过水解使果胶解聚，从而改变果胶的组成和结构并激活细胞壁防御。尽管已经报道了许多关于CWI的研究，但是关于PGs如何调节细胞壁免疫反应的机制尚不十分清楚。

结果

分the期在叶尖出现坏死，最终导致3–5 cm的黑褐色坏死组织。ltn-212显示出明显的细胞死亡和叶尖中H ₂ O _2的积累。在ltn-212中激活了防御反应，以抵抗水稻的细菌性枯萎病病原体。基于图的克隆显示，第一个内含子中的单个碱基取代（GA）导致OsPG1的错误剪接，从而导致坏死的表型。OsPG1在所有器官中组成性表达，并且在互补个体中恢复了野生型表型，并且敲除野生型系导致坏死，如ltn-212。透射电子显微镜显示，在ltn-212中细胞壁的厚度显着减少，细胞大小和形状显着减少。

结论

这些结果表明，OsPG1响应ltn-212的叶梢坏死表型而编码PG 。ltn-212的功能丧失突变破坏了CWI，导致自发性细胞死亡和自激活的防御反应，包括活性氧（ROS）爆发和发病相关（PR）基因表达，以及对黄单胞菌的增强抗性稻米pv 。稻（Xoo）。这些发现促进了我们对CWI介导的防御反应的理解。