Filamentous fungi can be found almost everywhere around the world including soil and food sources. They are capable of producing various secondary metabolites (SM) such as penicillin and carcinogenic mycotoxins. Aflatoxin B1 is the most notorious mycotoxins causing liver cancer which is produced by a filamentous fungus Aspergillus flavus. Although it has been shown at the genetic level that chromatin regulation is critical for controlling the expression of SM genes in fungi, a mechanistic view is not well-understood. In this work, a novel tetrameric histone modifying complex (“KERS” complex), containing JARID1-type H3K4 demethylase KdmB, putative cohesin acetyltransferase (EcoA), a class I type histone deacetylase RpdA and a ring finger protein StnB was discovered in model organism Aspergillus nidulans and pathogenic fungus Aspergillus flavus. Protein similarity analysis revealed that the KERS subunits are conserved from yeast to complex eukaryotes and mammals. The KERS complex couples chromatin regulation of SM gene clusters, fungal development, pathogenicity, and mycotoxin production. The KERS complex assembles in the nucleus and affects the expression of several gene clusters. The first part of this thesis addresses the role of KERS complex in A. nidulans. ecoA and rpdA are essential for A. nidulans viability. To study the functions of EcoA and RpdA in fungal light responses, promoters were replaced with tuneable Tet-ON constructs. KdmB and EcoA depletions resulted in increased sexual development indicating their role as negative-regulators of cleistothecia formation, while the loss of RpdA, and SntB completely abolished cleistothecia development presenting them as positive-regulators of sexual development. It was also shown that KdmB is required for EcoA protein stability, while SntB mediates EcoA proteasomal degradation to control nuclear levels. Post-translational modification analysis revealed that EcoA down-regulation results in the abrogation of conserved cohesin subunit yeast Smc3 ortholog SudA acetylation. Interdependence studies revealed that KdmB acts as a scaffold for binding EcoA to the heterodimer RpdA-SntB, whereas SntB recruits RpdA to the KdmB-EcoA heterodimer. Interestingly, SntB is required for the recruitment of RpdA to the KdmB-EcoA heterodimer, however, RpdA HDAC activity does not require functional SntB or KdmB. The second part of this work focuses on the role of KERS complex on pathogenic fungus A. flavus. The KERS complex was found to be conserved in A. flavus, comprising tetrameric KdmB, EcoA, RpdA, and SntB subunits. Similar to A. nidulans, ecoA was found to be essential for viability in A. flavus. In contrast with A. nidulans, rpdA was deleted successfully in pathogenic fungi. Developmental assays showed that both kdmB and rpdA are required for sclerotia production, aflatoxin biosynthesis and crop seed contamination in A. flavus through the nsdC, nsdD and afl pathways respectively. KdmB/RpdA affected the transcript levels of nearly 80% of the analysed secondary metabolism backbone gene clusters required for the transcription of polyketide synthetases (PKSs), non-ribosomal peptide synthetases (NRPSs) and dimethylallyl tryptophan synthetases (DMATs). It was also shown that both KdmB and RpdA regulate tri-methylation of H3K4me3 and H3K9me3 residues, while RpdA mainly acts on H3K14ac residues as well as H3K36me3. Hence, chromatin modifiers, KdmB and RpdA, are essential for fungal development, aflatoxin production and are key global regulators of SM gene clusters. The findings in this thesis provide insight into how chromatin modifier protein complexes can have broad effects on growth, development and natural product biosynthesis by regulating epigenetic marks. These results suggest that similar epigenetic mechanisms mediated by the KERS complex are likely conserved in eukaryotes, including pathogenic fungi. Thus, this study will provide support for the development of new strategies to reduce mycotoxin contamination, crop spoilage, disease and to improve yields of valuable fungal natural drugs which will benefit the pharmaceutical industry and improve economic growth.