Oren Parnas

As young man, even though enjoyed biology very much in high school, I was mainly interested in engineering and finance. I completed a B.Sc. degree in industrial engineering and management and then a M.Sc. in economics which I finished in 2001 at The Technion, Israel. During my studies I developed new mathematical approaches to price exotic options and started working in the analytics department of the financial division of Bank Hapoalim, the largest bank in Israel. After one year, I received an award for being an excellent employee of the finance division, selected out of 1,100 employees (2002), and in 2004 I was chosen to represent Israel and present new financial tools that I had developed at a European banking conference. My work in the bank developing analytical tools for the dealers in the trading room was very interesting and rewarding and I had tenure. While the materialistic advantages of my position were obvious, I did not feel fulfilled. I wished to explore and study nature and not work with “artificial systems”. I started to read basic literature and I was exposed to the complexity of cells tissues and organisms. I decided to take classes in biology at Tel Aviv University, in parallel to my work at the bank. Amazed by a fascinating course in genetics, I asked Prof. Martin Kupiec, the lecturer, if I could do a project in his lab. Every day after work at the bank, I went to the lab to work until around midnight, attracted by the intriguing and sophisticated world of genetics. After two years (2002-2004) working in the bank and studying biology in parallel, it was clear to me which I preferred and that I saw my future in science. I joined the Ph.D. program at the Life Science Faculty at Tel Aviv University under the supervision of Prof Kupiec. In my doctoral research I investigated the mechanisms that prevent genome instability, a hallmark of cancer. As a model we use the yeast Saccharomyces cerevisiae. I focused on Elg1, a protein that is involved in DNA replication, DNA repair, chromatin remodeling and sister chromatid cohesion. After I finished my Ph.D., I decided to change field and implement my approach to virology. I moved with my family to North Carolina to work on herpes viruses in Dr. Cullen's lab at Duke University, and received an EMBO long term fellowship. During my training I applied high throughput methods to find targets of miRNA, and was exposed to the field of genomics. My main project was to find the target of miRNAs that are encoded by herpes virus. After publishing a paper, I felt that my ability to develop to new areas and express myself was limited in that environment. This was an important test in my career and I believe that this period taught me how to cope with difficulties and how to overcome obstacles which are part of every scientific career. Following my desire for excellency, trusting my abilities and with my aspirations to be research scientist, after two years in Dr. Cullen's lab, I started a second post-doctoral training position in Dr. Regev's lab at the Broad Institute, aiming to contribute to the immunology field. When I started there in the beginning of 2014, the CRISPR revolution in mammalian genetics had already started, providing new tools to allow complete knockout of desired mammalian genes. This was an exciting opportunity to apply and further develop the methodology that I had used in lower eukaryotes during my Ph.D., now in mammalian cells that are part of the immune system. I decided to perform a genome-wide CRISPR screen in immune cells, and chose dendritic cells which provide a bridge between the innate and the adaptive immune systems and have an important role in control of pathogens and cancer. I thought that combining genetic and genomic studies would enable the discovery not only of which genes and proteins are changed in immune cells during the immune response, a well-studied question in the Regev lab, but also which genes are essential for the response. I became expert in all stages of the screen including both the experimental and the computational parts. This work led to performing a genome-wide CRSPR screen in primary immune cells and was the first use of protein expression as a phenotypic readout for the screen. In new work published in December 2016, I extend this methodology and together with colleges in the Regev lab developed a method named Perturb-seq, which enables to find new the genetic interactions between set of genes. In Perturb-seq we are using single cell RNA-seq of CRISPR perturb cells to find the effect of combinations of perturbations on the transcription profile. On July 2016 I start new position as principal investigator in the Hebrew university, Jerusalem, Israel, exploring the interactions between the immune system and cancer.