My lab studies the epigenetic mechanisms by which chromatin regulates gene expression and DNA replication. Recently we have embarked on the analysis of how and when genes switch on and off as directed by chromatin structure. Our primary goal is to link this type of regulation to the overhaul and reassembly of chromatin after the passing of DNA replication forks. These mechanisms of gene regulation and epigenetic inheritance are highly conserved between eukaryotes. Hence, the gained knowledge spans broadly to the fields of genetic disease and cancer, to parasite immune evasion and to the adaptation of organisms to the environment. Separately, I conduct research on education and student performance in higher level university courses. Education B.Sc. - Sofia, Bulgaria Ph.D. - Imperial Cancer Research Fund, London, England

Telomeres: epigenetics, gene repression and genome plasticity. We use the telomeres of the yeasts S.cerevisiae as a model for the analyses of gene repression and epigenetic inheritance. Telomeres are repetitive sequences at the ends of eukaryotic chromosomes. They confer the formation of repressive chromatin structures and exert strong gene repression signals. Interestingly, the length of telomeres and their structure have been implicated in longevity and in the regulation of genome stability. In addition, the genes that are positioned close the telomeres of S.cerevisiae(and to the telomeres of many other eukaryotes) convert between repressed and active states. We call these on-off switches. Ongoing studies focus on the possible role of dormant origins of DNA replication and associated factors in the epigenetic convertibility of genes. Using this simple model organism, we are attempting to decipher general principles of gene repression and its links to DNA replication. DNA replication. DNA replication is tightly controlled to allow exactly one round of duplication of the genome in each cell cycle. In eukaryotes, this control is exerted through factors, which confer one single firing of defined origins of DNA replication. We know reasonably well how these factors operate. However, we do not know how these factors communicate with the complex chromatin environment in the eukaryotic nuclei. We are focusing on the origins in the vicinity of telomeres to address these questions.

Jeffery, D., Naoko, K., You, Z., Gharib, M., Wyse, B., Drury, E., Weireich, M., Thibault, P., Verreault, A., Masai, H., Yankulov, K. (2015). CDC28 regulates the association of Chromatin Assembly Factor I with chromatin. Cell Cycle, 14 (01), 74 - 85. Jeffery, D., Wyse, B., Muhammad, R., Brown, G., You, Z., Oshidari, R, Masai H, Yankulov K (2013). Analysis of epigenetic stability and conversions in Saccharomyces cerevisiae reveals a novel role of CAF-I in position-effect variegation. Nucleic Acids Research, 41 (18), 8475-88. Wyse, B., Oshidary, R., Jeffery, D., & Yankulov, K. (2013). Parasite epigenetics and immune evasion: lessons from budding yeast. Epigenetics & Chromatin, 19;6(1):40. doi: 10.1186/1756-8935-6-40. Power, P., Jeffery, D., Rehman, M. A., Chatterji, A., & Yankulov, K. (2011). Sub-telomeric core X and Y' elements in S. cerevisiae suppress extreme variations in gene silencing. PLoS ONE. 6(3):e17523. doi: 10.1371/journal.pone.0017523 Rehman MA, Wang D, Fourel G, Gilson E, Yankulov K. Subtelomeric ACS-containing proto-silencers act as antisilencers in replication factors mutants in Saccharomyces cerevisiae. (2009) Mol. Biol. Cell 20:631-41.