I have always been interested in how gene expression is regulated. After my PhD in virus-host interactions, I moved into the world of functional genomics by joining Prof. Julie Ahringer’s group at the Gurdon Institute, University of Cambridge. Working with modENCODE consortium, my work in Cambridge greatly improved our knowledge of C. elegans promoter and enhancer architectures by mapping transcription start sites using capRNA-seq and by examining chromatin features using ChIP-seq. Most excitingly, my previous research provided the first evidence demonstrating that CpG-rich promoters in C. elegans display similar chromatin features with human CpG island promoters (e.g. high chromatin accessibility) This finding is unexpected as CpG islands have been considered to be a vertebrate-centric feature (in more than 50 % of human promoters). In addition to that, the high conservation of chromatin factors and the ease of genetic manipulation and molecular experiments, make C. elegans a great system to study chromatin function that is relevant to human diseases.

The main objective of our research programme is to understand chromatin function and gene regulation. DNA wraps around histones to form chromatin. This protein-nucleic acid complex protects DNA from damage and plays a role in controlling the accessibility of the genetic information encoded in the genome. For instance, open chromatin is often a feature of active promoters where the transcription machinery is able to read the genetic code for producing RNA transcripts. In contrast, closed/compact chromatin structure is often found in repressed regions. The open and closed states of chromatin structure are interchangeable and tightly regulated by chromatin regulatory complexes. Many chromatin factors remain unstudied. Defects in chromatin function frequently lead to severe defects such as human cancer. Therefore, a better understanding of chromatin structure and regulation will shed light on potential therapeutic treatments for human diseases.