Jarad Mai, Mariappan Kiruthiga, Almeida-Trapp Marilia, Mette Michael Florian, Mithöfer Axel, Rayapuram Naganand, Hirt Heribert
DARWIN21, Biological and Environmental Sciences and Engineering Division (BESE), King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia.
Research Group Plant Defense Physiology, Max Planck Institute for Chemical Ecology, Jena, Germany.
Front Plant Sci. 2020 Jan 9;10:1639. doi: 10.3389/fpls.2019.01639. eCollection 2019.
Pathogen-associated molecular pattern (PAMP) recognition occurs by plasma membrane located receptors that induce among other processes nuclear gene expression. However, signaling to the nuclear compartment is restricted by the nuclear envelope and nuclear pore complexes. We show here that among the four lamin homologs LITTLE NUCLEI/CROWDED NUCLEI (LINC/CRWN), LINC1 plays an important role in PTI and jasmonic acid (JA) signaling. We show that knock out mutants affect PAMP-triggered MAPK activation and growth inhibition, but not reactive oxygen species or callose accumulation. We also demonstrate that mutants are compromised in regulating PAMP-triggered pathogen-related genes, in particular encoding factors involved in JA signaling and responses. Expression of a number of JAZ domain proteins, the key JA-related transcription factor MYC2 as well as key MYB transcription factors and biosynthesis genes of both the indole and aliphatic glucosinolate pathways are changed in mutants. Moreover, PAMP triggers JA and JA-Ile accumulation in mutants, whereas salicylic acid levels are unchanged. Despite impairment in PAMP-triggered immunity, mutants still show basal immunity towards DC3000 strains. High JA levels usually render plants resistant to necrotrophic pathogen. Thus, mutants show enhanced resistance to infection. In accordance with a general role of LINC1 in JA signaling, mutants are hypersensitive to growth inhibition to external JA. In summary, our findings show that the lamin-like LINC1 protein plays a key role in JA signaling and regulation of PTI responses in .
病原体相关分子模式（PAMP）识别是通过位于质膜上的受体发生的，这些受体可诱导包括核基因表达在内的多种过程。然而，向核区室的信号传导受到核膜和核孔复合体的限制。我们在此表明，在四个核纤层蛋白同源物小核/密集核（LINC/CRWN）中，LINC1在植物病原体侵染初期（PTI）和茉莉酸（JA）信号传导中起重要作用。我们发现敲除突变体影响PAMP触发的丝裂原活化蛋白激酶（MAPK）激活和生长抑制，但不影响活性氧或胼胝质积累。我们还证明，突变体在调节PAMP触发的病原体相关基因方面存在缺陷，特别是那些编码参与JA信号传导和反应的因子。许多JAZ结构域蛋白、关键的JA相关转录因子MYC2以及吲哚和脂肪族芥子油苷途径的关键MYB转录因子和生物合成基因在突变体中的表达发生了变化。此外，PAMP在突变体中触发JA和茉莉酸异亮氨酸（JA-Ile）积累，而水杨酸水平不变。尽管在PAMP触发的免疫中存在缺陷，但突变体对DC3000菌株仍表现出基础免疫。高JA水平通常使植物对坏死营养型病原体具有抗性。因此，突变体对感染表现出增强的抗性。与LINC1在JA信号传导中的一般作用一致，突变体对外部JA的生长抑制高度敏感。总之，我们的研究结果表明，核纤层样LINC1蛋白在JA信号传导和拟南芥PTI反应调控中起关键作用。
