1. Epigenetic switch
1.1. Effectors L. maculans
1.1.1. Involving H3K9me3
1.2. (Avr) gene aid pathogen infection
1.2.1. Mutation / Multiple translocation
1.2.1.1. Escape host immunity and become virulent again
1.3. Allow reuse / recycling of effectors
2. sRNA
2.1. Functions at the post-transcriptional level
2.2. Regulates cellular and developmental process
2.3. Post-transcriptional gene silencing (PTGS) associates with the components of RNAi for gene silencing
2.3.1. Dicer-like genes such as MoDcl1 and MoDcl2 of M. oryzae show functional diversity
2.3.1.1. MoDcl1 produces siRNAs when overexpressed in the MoDcl2 knockout mutant
2.3.1.2. MoDcl2 is independent of MoDcl1 in RNA silencing
2.4. Targets homologous DNA sequence and modifies chromatin for heterochromatin assembly and gene silencing together with RNAi
2.5. sRNA profile of pathogen is altered depending on physiological stress and host conditions
2.6. sRNA biosynthetic mutants of Dicer-like genes and RdRP genes shows an increase in the transcription of subsets of genes of M. oryzae
2.7. Three kinds of RNA-i dependent gene silencing mechanism
2.7.1. Heterochromatin Formation
2.7.1.1. Large part of genome that are tightly packed into highly condensed regions
2.7.1.2. Maintain genome integrity and gene silencing within or close to heterochromatic region
2.7.1.3. Heterochromatic Protein (HP1) or yeast homologue SWI6 aid H3K9me in triggering gene silencing
2.7.1.4. Some fungus has exosome as RNA-based regulatory mechanism
2.7.1.4.1. Function in degrading aberrant RNA
2.7.1.4.2. Aid in heterochromatin formation
2.7.1.4.3. Shuttle RNA that are also known as endogenous short RNAs (esRNAs) between cells
2.7.2. Quelling
2.7.2.1. Homology silencing mechanism
2.7.2.1.1. Silences native sequence homologous to transformed DNA in vegetative tissues
2.7.2.2. RNAi silencing mechanism induced by aberrant RNA
2.7.2.3. Affects heterochromatin formation and gene regulation
2.7.3. Meiotic silencing by unpaired DNA (MSUD)
2.7.3.1. RNAi dependent silencing mechanism in N. crasso
2.7.3.2. Occur at sexual developmental stage
2.7.3.3. Unpaired DNA initiates silencing of the unpaired DNA itself and its homologues
2.7.3.4. Trigger the production of aberrant RNA specific to the unpaired DNA which is converted to dsRNA by a group of proteins
2.7.3.4.1. dsRNA is cleaved via Dcl1 into 20-25 nucleotide sRNAs before binding to suppressor of meiotic silencing and QIP (an exonuclease) that leads to post transcriptional silencing of homologues genes
2.7.3.5. Not prevalent in fungal plants pathogens
3. UNEXPLORED ASPECTS OF EPIGENETICS
3.1. Secondary metabolites
3.1.1. Melanin
3.1.1.1. Helps create high turgor pressure for fungal penetration into plant cell wall
3.1.2. MoAcat1 and MoAcat2
3.1.2.1. Catalytic enzyme of mevalonate pathway
3.1.2.1.1. Give rise to isoprenoids
4. EPIGENETIC BASIS OF EVOLUTION, HOST-PATHOGEN INTERACTIONS AND EPIDEMIC EPIDEMIOLOGY
4.1. Determination pattern of histone methylation in different geographical fungal could help trace evolutionary history and spread of fungal disease
4.2. Target recognition domain (TRD) of DNMTs recognize specific DNA sequence patterns for methylation
4.2.1. Alter methylation pattern by moving between and sometimes within genes
4.3. M. oryzae possess DNA methylation for small portion of cytosine sites with low methylation levels
4.3.1. Action of evolutionary selection forces and role of methylome appear ambiguous
4.4. Control virulence through regulation of TEs
4.4.1. Play a role in phenotypic diversification and host-pathogen co-evolution
4.5. Changes in the effector proteins of fungal pathogens aid in the evasion of host immunity
4.5.1. Regulated by sequence alterations or loss-of-virulence genes
4.5.2. Transgenerational epigenetic aids in evading host defence mechanisms
5. DNA Methylation
5.1. RIP mutation
5.1.1. Mechanism of gene silencing (Defence system)
5.1.1.1. Repeated sequences shown to affect DNA Methylation status
5.1.1.1.1. RIP'd sequences mostly associated with cytosine methylation during sexual stages
5.2. 5mc
5.2.1. Dynamic (TE-rich regions)
5.2.1.1. Global genome/Transposable elements (MAGGY retrotransposons)
5.2.1.1.1. Evolutionary role-ambiguous
5.2.1.2. MoDMT1
5.2.1.2.1. Phenotypic analysis show no significant role in regulation of development and pathogenicity
5.2.1.3. mC site in mycelia clustered into densely methylated domains around transposable element (indicate TE region targeted for DNA Methylation)
5.3. DNMT (Enzyme)
5.3.1. Catalyse methylation of cytosine bases (Eukaryote)
5.3.1.1. DNMT1
5.3.1.1.1. Maintain the methylated state
5.3.1.2. DNMT2 / DNMT 3
5.3.1.2.1. (DNMT3) Involve in development of methylation pattern
5.4. Dynamic nature depends on fungal/strain types, growth condition and stage
6. Histone Modifications & Variants
6.1. Histone acetylation & deacetylation
6.1.1. Histone acetylation
6.1.1.1. Regulates by
6.1.1.1.1. Histone acetyltransferases (HATs)
6.1.1.1.2. Histone deacetyltransferases (HDACs)
6.2. Histone methylation & demethylation
6.2.1. Histones methyl transferases (HMTs) - responsible for lysine and arginine residues on histone proteins Histone demethylase (HDM) - reverse the methylation process
6.2.1.1. Methylation of arginine residues occurs at H3R2, H3R8, H3R17, H3R26 and H4R3 sites
6.2.1.2. The degree of specificity of lysine methylation [mono (me1), di (me2), tri (me3)
6.2.1.2.1. Responsible for transcriptional activation and repression of the gene
6.2.1.3. In M. oryzae
6.2.1.3.1. Histone methylation has been associated with gene activation and repression
6.2.1.3.2. The substrate induced activation of cellulase gene mediated through histone methylation
6.2.1.3.3. MoSeT1
6.2.1.3.4. In deletion mutant of MoSET1