^{5th International Congress on} Epigenetics & Chromatin August 22-23, 2019 Vienna, Austria

Richard Y C Kong has completed his PhD at Monash University, Australia and Postdoctoral research at the University of Hong Kong, Hong Kong SAR, China. He is presently an Associate Professor at the City University of Hong Kong and has published more than 80 papers in internationally referred and reputed journals His research interest is  on the development and application of novel DNA-based technologies as risk assessment and bioremediation tools to address problems related to diverse aspects of pollution in the marine environment.

Statement of the Problem: Hypoxia is a pressing environmental problem aff ecting marine and freshwater ecosystems worldwide Hypoxia was found to cause severe reproductive impairments in fi sh, leading to heavy loss of fisheries production over large areas. Laboratory and fi eld studies demonstrated that hypoxia can aff ect both male and female

reproductive systems For example, hypoxia was found to suppress spermatogenesis and decrease sperm motility in carp, impair testicular development and sperm production, and reducing reproductive success in Atlantic croaker retardation of gonadal development has also been observed in the ovaries of female fish numerous reports attributed the reproductive impairments to the suppression of steroidogenic gene expression and alteration of sex hormone production in fish gonads. However, not much is known about the diff erential gene responses in gonads of male and female fi sh to hypoxia stress.The purpose of this study is to investigate the eff ects of hypoxia on the molecular gene responses in the gonads of male and female marine medaka fish.

Methodology: We conducted mRNA transcriptome sequencing and histology on ovaries and testes of hypoxia-exposed marine medaka (Oryzias melastigma) fish, followed by bioinformatics analysis with the view to determining the nature of the molecular responses of male and female fish gonads to hypoxic stress Functional Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Ingenuity Pathway (IPA) analyses were carried out.

Findings: Bioinformatic and functional analyses demonstrated differential and gender-specifi c expression of signaling pathways affecting specifi c biological functions in response to hypoxic stress that correlated with the impairment of reproductive functions in hypoxia-exposed male and female fish.

Conclusion & Significance: Our data provided valuable insights into the diff erential and possible transgenerational molecular responses triggered by chronic hypoxic stress in marine fish.

Richard Meehan is a genetics graduate of TCD (Dublin) and has been studying DNA methylation dynamics for over 25 years. Research landmarks include the identifi cation of methyl-CpG binding proteins (MeCP1 and MeCP2), non-catalytic roles for DNMT1 and alternate hypotheses regarding DNA methylation reprogramming in development and disease states. He is currently a Professor at the MRC Human Genetics Unit in Edinburgh and investigating how 5 hydroxymethylcytosine profi ling can be used as a cell identifi er.

The complex chromatin environment of a single nucleus is a combinatorial outcome of a cells developmental history and the dynamic interplay between competing DNA and histone modifi cation pathways that act to reinforce stable

transcriptional states. Cell potency is initially established by signalling pathways and activation of pluripotent Gene Regulatory Networks (GRNs) in early embryogenesis; as development proceeds there is a programmed restriction in cell

fate choices that coincides with the establishment of and dependence upon repressive epigenetic silencing mechanisms. Our work suggests that two mutually exclusive repression pathways DNA methylation and polycomb, impacts on their

respective deposition in stem cell models. We fi nd that DNA methylation directs the formation of polycomb dependent higher order chromatin structure in stem cells and early development, conversely polycomb can direct patterns of DNA

methylation at discrete genomic regions. Author will discuss the impact of these mechanisms on stem cell potency and how these interactions are linked with the occurrence of altered epigenetic states in disease.