Abstract
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 Arabidopsis lamin homologs LITTLE NUCLEI/CROWDED NUCLEI (LINC/CRWN), LINC1 plays an important role in PTI and jasmonic acid (JA) signaling. We show that linc1 knock out mutants affect PAMP-triggered MAPK activation and growth inhibition, but not reactive oxygen species or callose accumulation. We also demonstrate that linc1 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 linc1 mutants. Moreover, PAMP triggers JA and JA-Ile accumulation in linc1 mutants, whereas salicylic acid levels are unchanged. Despite impairment in PAMP-triggered immunity, linc1 mutants still show basal immunity towards Pseudomonas syringae DC3000 strains. High JA levels usually render plants resistant to necrotrophic pathogen. Thus, linc1 mutants show enhanced resistance to Botrytis cinerea infection. In accordance with a general role of LINC1 in JA signaling, linc1 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 Arabidopsis.
Highlights
Plants are constantly under attack from potentially pathogenic microbes
LINCs contain a tripartite structure with a central coiled coil domain as well as nuclear localization signals and are proposed to be the best candidates of lamins in Arabidopsis (Guo and Fang, 2014). They have been shown to participate in functions such as in regulating chromatin organization and nuclear shape and size that are controlled by nuclear lamins in organisms other than plants
To elucidate the specific role of LITTLE NUCLEI1 (LINC1) in the pattern-triggered immunity (PTI) stress response, we investigated whether LINC1 is involved in flg22-induced PTI responses
Summary
Plants are constantly under attack from potentially pathogenic microbes. The perception of a pathogen attack by the plant triggers the activation of immune signaling events and defense responses. Defense responses include a rise in the intracellular calcium concentration (Liese and Romeis, 2013), the production of reactive oxygen species (ROS) (Torres et al, 2006), the activation of mitogen-activated protein kinase (MAPK) cascades and the expression of pathogen-related proteins (Nurnberger et al, 2004; Ahuja et al, 2012), and the biosynthesis of stress-related hormones such as salicylic acid (SA), jasmonic acid (JA), and ethylene (Grant and Jones, 2009; Tsuda et al, 2013) These early events after PAMP perception lead to defense responses mediated by transcriptional reprogramming (Mur et al, 2008), stomatal closure, production of antimicrobial compounds (Dixon, 2001), and the deposition of callose (Gomez-Gomez et al, 1999). Effector-triggered immunity is prompted when effectors transferred by host-adapted pathogens in order to interrupt signaling steps of the PTI response are recognized by Resistance proteins of the host cells (Jones and Dangl, 2006; Nicaise et al, 2009; Collier and Moffett, 2009; Dodds and Rathjen, 2010; Tsuda and Katagiri, 2010; Hann et al, 2010; Spoel and Dong, 2012; Takken and Goverse, 2012)
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