Gil Ast

Gil Ast's lab has made several breakthrough contributions in the field of alternative splicing evolution and discovered two out of three demonstrated mechanisms for the origin of alternative exons (i.e., Alu exonization and exons that changed their mode of splicing from constitutive to alternative during evolution). Furthermore, his group has identified most of the known evolutionary forces that determine the choice of alternative exons. They have also identified a potential therapy for a neurodegenerative splicing disease, Familial Dysautonomia, currently undergoing clinical trials at NYU with very promising mid-term results. They identified how chromatin organization (nucleosome occupancy) and epigenetics (histone modifications and DNA methylation) regulate alternative splicing. Ast and his co-workers have published numerous studies in leading journals, revealing, for example, how the human genome obtained some of its unique characteristics, how new mRNA isoforms have emerged during evolution and gained novel functions, how chromatin structure and other epigenetic determinants can regulate the splicing reaction, and the links between alternative splicing and certain genetic disorders and cancer. His lab was one of the first in the world to integrate computational biology and experimental bench work. Their mastery of both bioinformatics and molecular biology approaches enables the multidisciplinary work that has led to unique contributions. His group is highly productive and uniquely positioned in the field of RNA processing.