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Mechanisms of Epigenetics Modifications in Magnaporthe oryzae, A clear…

- - - - The genomic sequences of both the fungus (M. oryzae) and its main host (rice) are accessible, making this pathosystem genetically and experimentally tractable, which makes it easier to study how hosts and pathogens interact.
        
        Enabling the development of fungal pathogen prevention and control techniques.
  - - - Some fungal avirulence (Avr) genes encode virulence factors which call effector proteins.
        
        To overcome immunity and reactivate their virulence, Avr genes will mutate or experience many translocations.
        
        Variations in the balance of epigenetic factors can impact transposon activity or Avr gene expression, ultimately leading to alterations in virulence.
    - - In M. oryzae, it has been demonstrated that secondary metabolites; melanin, contribute significantly to fungal pathogenicity
        
        Melanin, a pigment with a dark color that contributes to the strong turgor pressure necessary for fungi to penetrate plant cell walls, is a derivative of the phenolic precursor.
        
        Mutations in M. oryzae that lack melanin results in non-pigmented appressoria that cannot pierce the epidermal cells of the leaf cuticle.
        
        The M. oryzae homologs of the acetoacetyl CoA gene, an essential catalytic enzyme of the mevalonate pathway, are known as MoAcat1 and MoAcat2.
        
        M. oryzae virulence and vegetative development (plus virulence) depend on MoAcat1's mitochondrial localization and MoAcat2's cytoplasmic localization.
    - - Only a small percentage of the cytosine sites in M. oryzae DNA have been methylated, and the levels of methylation are modest.
        
        As a result, it is unclear whether the methylome will ultimately play a significant role in promoting adaptive evolution.
- - - - MoDcl1
        
        produces siRNAs when overexpressed in the MoDcl2 knockout mutant,
      - MoDcl2
        
        involved in RNA silencing independent of MoDcl1
      - What Dicer does?
        
        cleaves the double-stranded RNA (dsRNA) into 20–30-bp-long small interfering RNAs (siRNAs), which are loaded onto the RNA-induced silencing complex (RISC), which triggers the degradation or translational inhibition of the target mRNA.
  - - - because there is alternative mechanisms of RNA-based silencing.
      - What is quelling?
        
        A homology-dependent gene silencing mechanism that silences the native sequence homologous to transformed DNA in vegetative tissues.
        
        It is an RNAi-dependent silencing mechanism induced by aberrant RNA.
        
        It is known to affect heterochromatin formation and gene regulation.
    - - It does not seem to be prevalent in fungal plant pathogens because the dominant prevalence of the sexual phase has not been reported under natural conditions.
      - What is MSUD?
        
        Another RNAi-dependent silencing mechanism discovered in N. crassa.
        
        Occur at the sexual developmental stage when the unpaired DNA initiates silencing of the unpaired DNA itself and its homologues
- - - - Lysine
        
        Histone core H3 - K79
        
        H4 tail - K20
        
        N-terminal - K4, K9, K27, K36
      - Arginine
        
        H3R2, H3R8, H3R26, H4R3
    - - HMTs
        
        responsible for methylation of lysine and argenine residues on histone protein.
      - HDM
        
        Lysine histone demethylase ( LSD1 ) - reverse methylation process.
    - - Methylation of H3K4 at MoCel7C locus by activation of MoCel7C gene
      - Disruption of MoSET1 severely impaired conidiation and appressorium formation and rendering the strain ineffective in causing disease in host plant.
  - - - HDACs antagonize HATs by removing acetylatioon from amino group of lysine residue.
        
        Thus lysine positive charge restored
        
        Underlying DNA sequences coil and wind up tightly to histone and become inaccessible.
    - - HDAC
      - HAT
    - - group histone modifying enzymes (HMEs) based ion domain structure and other criteria.
    - - Treatmentment of M oryzae with HDACs inhibitors of Rpd3/Hda1 resulted in inhibition of appressorium formation and decreased pathogenicity.
        
        indicate HDAC significant role in asexual differentiation of M. oryzae
      - Homologies of the transducin beta-like gene TIG1 (conserved HDACs trnascriptional corepressor complex)
        
        important for pathogenicity and conidiogenesis
        
        Deletion will rendered the mutant hypersensitive to oxidative stress thus forming invasive hyphae
        
        when associated with purified protein complexes result in identification of two HDACs (homologous to Set3 complex in yeast.
      - TWL (twilight)
        
        for asexual development and pathogenesis
        
        facilitates pathogen attack on the host system