ABSTRACT
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.
Subject(s)
DNA (Cytosine-5-)-Methyltransferases/genetics , Drosophila Proteins/genetics , Drosophila melanogaster/enzymology , Drosophila melanogaster/genetics , Gene Expression Regulation , Genomic Instability , Interspersed Repetitive Sequences/genetics , Amino Acid Sequence , Animals , Base Sequence , Biocatalysis , DNA (Cytosine-5-)-Methyltransferases/chemistry , DNA (Cytosine-5-)-Methyltransferases/metabolism , DNA Methylation/genetics , DNA Transposable Elements/genetics , Drosophila Proteins/chemistry , Drosophila Proteins/metabolism , Female , Gene Silencing , Genetic Loci , Heat-Shock Response/genetics , Male , RNA Stability , RNA, Transfer/genetics , Transcriptome/genetics , Y Chromosome/geneticsABSTRACT
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.
Subject(s)
Arabidopsis Proteins/metabolism , Arabidopsis/metabolism , Arabidopsis/microbiology , Plants, Genetically Modified/metabolism , Plants, Genetically Modified/microbiology , Arabidopsis/genetics , Arabidopsis Proteins/genetics , Botrytis/pathogenicity , Plant Immunity , Plants, Genetically Modified/genetics , Protein Serine-Threonine Kinases/genetics , Protein Serine-Threonine Kinases/metabolism , Signal Transduction/genetics , Signal Transduction/physiologyABSTRACT
Due to their economic relevance, the study of plant pathogen interactions is of importance. However, elucidating these interactions and their underlying molecular mechanisms remains challenging since both host and pathogen need to be fully genetically accessible organisms. Here we present milestones in the establishment of a new biotrophic model pathosystem: Ustilago bromivora and Brachypodium sp. We provide a complete toolset, including an annotated fungal genome and methods for genetic manipulation of the fungus and its host plant. This toolset will enable researchers to easily study biotrophic interactions at the molecular level on both the pathogen and the host side. Moreover, our research on the fungal life cycle revealed a mating type bias phenomenon. U. bromivora harbors a haplo-lethal allele that is linked to one mating type region. As a result, the identified mating type bias strongly promotes inbreeding, which we consider to be a potential speciation driver.
Subject(s)
Brachypodium/genetics , Brachypodium/microbiology , Host-Pathogen Interactions , Molecular Biology/methods , Ustilago/genetics , Ustilago/physiology , Genes, Mating Type, FungalABSTRACT
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.
