The maintenance of eukaryotic genome stability is ensured by the interplay of transcriptional as well as post-transcriptional mechanisms that control recombination of repeat regions and the expression and mobility of transposable elements. We report here that mutations in two (cytosine-5) RNA methyltransferases, Dnmt2 and NSun2, impact the accumulation of mobile element-derived sequences and DNA repeat integrity in Drosophila. Loss of Dnmt2 function caused moderate effects under standard conditions, while heat shock exacerbated these effects. In contrast, NSun2 function affected mobile element expression and genome integrity in a heat shock-independent fashion. Reduced tRNA stability in both RCMT mutants indicated that tRNA-dependent processes affected mobile element expression and DNA repeat stability. Importantly, further experiments indicated that complex formation with RNA could also contribute to the impact of RCMT function on gene expression control. These results thus uncover a link between tRNA modification enzymes, the expression of repeat DNA, and genomic integrity.
Pathogen-responsive mitogen-activated protein kinase (MAPK or MPK) cascades relay signals from activated immune receptors across the nuclear envelope to intranuclear targets. However, in plants, little is known about the spatial control of MAPK signaling. Here, we report that the Arabidopsis (Arabidopsis thaliana) nuclear pore complex protein Nup88/MOS7 is essential for immunity to the necrotrophic fungus Botrytis cinerea The mos7-1 mutation, causing a four-amino acid deletion, compromises B. cinerea-induced activation of the key immunoregulatory MAPKs MPK3/MPK6 and reduces MPK3 protein levels posttranscriptionally. Furthermore, MOS7 contributes to retaining a sufficient MPK3 abundance in the nucleus, which is required for full immunity to B. cinerea Finally, we present a structural model of MOS7 and show that the mos7-1 mutation compromises interactions with Nup98a/b, two phenylalanine-glycine repeat nucleoporins implicated in maintaining the selective nuclear pore complex permeability barrier. Together, our analysis uncovered MOS7 and Nup98 as novel components of plant immunity toward a necrotrophic pathogen and provides mechanistic insights into how these nucleoporins coordinate nucleocytoplasmic transport to mount a robust immune response.
Arabidopsis nucleoporin MOS7/NUP88 was identified in a forward-genetic screen for components that contribute to auto-immunity of the deregulated Resistance (R) gene mutant snc1, and is required for immunity to biotrophic and hemi-biotrophic pathogens. In a recent study, we showed that MOS7 is also essential to mount a full defense response against the necrotrophic fungal pathogen Botrytis cinerea, suggesting that MOS7 modulates plant defense responses to different types of pathogenic microbes. Here, we extend our analyses of MOS7-dependent plant immune responses and report the genetic requirement of MOS7 for manifestation of phenotypes associated with the CHITIN ELICITOR RECEPTOR KINASE1 (CERK1) mutant cerk1-4. KEYWORDSArabidopsis immunity; cell death; cerk1-4; LysM-RLK; NUP88/MOS7; nucleoporin; nucleocytoplasmic transport; PRRThe plant innate immune system relies on 2 major classes of immune receptors to detect pathogens and activate downstream defense responses. At the plasma membrane, pattern recognition receptors (PRRs) recognize conserved pathogen-or microbe-associated molecular patterns (PAMPs/MAMPs) such as fungal chitin via extracellular ligand binding domains, whereas intracellular nucleotide-binding site leucine-rich repeat receptors (NLRs) perceive the action of specific pathogen effector molecules. 1 Cellular defense signaling upon activation of both immune receptor classes involves the relay of stress stimuli into the nucleus to alter the expression of immune response genes. [2][3][4] The macromolecular exchange across the nuclear envelope (NE) is regulated by nuclear transport receptors (NTRs) and nuclear pore complexes (NPCs) composed of nucleoporins (Nups). 5,6 In Arabidopsis, the NUP88 homolog MOS7 (MODIFIER OF SNC1, 7) was first identified in a forward-genetic screen for positive regulators of auto-immunity activated in the deregulated Toll-Interleukin Receptor (TIR)-type NLR mutant suppressor of npr1-1, constitutive1 (snc1). 7 Whereas snc1 plants are dwarf, accumulate high levels of the defense hormone salicylic acid (SA), constitutively express PATHOGENESIS RELATED (PR) genes and show enhanced resistance to virulent biotrophic and hemi-biotrophic pathogens, 8,9 these phenotypes are abolished in snc1 mos7-1 double mutant plants. 7 Subsequent analyses showed that mos7-1 single mutants are impaired in nuclear retention of auto-active SNC1 as well as the SA response regulators ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and NONEXPRESSOR OF PATH-OGENESIS-RELATED GENES1 (NPR1). Accordingly, mos7-1 shows defects in SA-, EDS1-and NPR1-dependent immunity to virulent and avirulent isolates of the biotrophic oomycete Hyaloperonospora arabidopsidis and the hemi-biotrophic bacterium Pseudomonas syringae. 7,10 More recently, we uncovered that MOS7 is also essential for establishing a full defense response against the gray mold fungus Botrytis cinerea, a necrotrophic pathogen that kills its host plants. 11 When co-expressed transiently in leaves of Nicotiana benthamiana, MOS7 interacts with NUP98a and N...
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