Dr. Matan Sorek

Dr. Matan Sorek
Dr. Matan Sorek
Israeli Postdoctoral Scholar
2022-2023 Cohort
University of Pennsylvania
Department of Biology
  • Berger Lab
  • Shelley Berger Lab website

Matan Sorek tested a provocative hypothesis for his PhD in Brain Sciences at The Hebrew University: the deleterious effects of the neurodegenerative disorder Huntington’s disease (HD) can be explained by changes in gene expression variability between diseased and healthy cells, rather than as a result of complete disruption of biological processes.

Later, as a research associate, he became interested in Transposable Elements (TEs), a topic he returns to with his postdoc. Widespread in the genome of most animals, TEs are mobile DNA sequences involved in development as well as in aging and inflammation. These sequences can also serve as transcriptional enhancers to nearby genes, making them potential targets for the induction (activation) of the global transcriptional switches that allow genes to be expressed at the appropriate time. In his earlier study, Dr. Sorek analyzed expression of TEs in response to SARS-CoV2 infection. He found that while other viruses cause a significant induction of TEs, alerting the immune system response, SARS-CoV2 operates “under the radar” and causes much less TE induction.

Dr. Sorek continues his research as a postdoc at the University of Pennsylvania’s Epigenetics Institute, which studies how behavior and environment affect the way genes work. He studies the C. floridanus ant which, in addition to queen and males, has two worker castes: Major workers have larger body size and defend the colony, while Minor workers provide nursing and foraging. Both castes contain the same DNA, so scientists believe epigenetic regulation must underlie this specialization. Indeed, young ants from the Major caste can be reprogrammed to show Minor-like foraging by epigenetically manipulating gene expression in their brains. Dr. Sorek analyzes and manipulates TE expression levels in the ants to shed further light on TE’s role in these epigenetic differences.