Gil Ast

Research Focus

The long term objectives of our lab are to understand how alternative splicing create primate-specific genomic diversity; how alternative splicing and the birthing process of new exons in the human genome are linked to genetic disorders and cancer; and what are the evolutionary process that create alternative splicing, and whether this process responsible for higher order of phenotypic complexity.

Our research combines bioinformatics and molecular biology tools to uncover the following aims: (1) How many primate-specific exons we have in the human genome and which contribute to some of the unique features of humans. (2) Whether formation of new exons due to somatic mutations involve in cancer. (3) What are the evolutionary forces that shape the human transcriptome? (4) What is the evolution of alternative splicing?

Publications

1. Kol, G., Lev-Maor, G., Ast, G. (2005) Human-Mouse Comparative Analysis reveals that Branch-site plasticity contributes to splicing regulation. Human Molecular Genetics. 14:1559-1568.
2. Shomron, N., Alberstein, M., Reznik M. and Ast, G. (2005) Stress alters the subcellular distribution of hSlu7 and modulates alternative splicing. J. Cell Science 118: 1151-1159.
3. Sorek R., Lev-Maor G., Reznik M., Dagan T., Belinky F., Graur D., Ast G. (2004) Minimal conditions for exonization of intronic sequences: 5’ splice site formation in Alu exons. Mol. Cell. 14(2):221-231.
4. Ast G. (2004) How did alternative splicing evolve? Nature Reviews Genetics. 5(10):773-782.
5. Lev-Maor, G., Sorek, R., Shomron, N., Ast, G. (2003) The birth of an alternatively spliced exon: 3' splice-site selection in Alu exons. Science. 300:1288-1291.

Key lab techniques: Comparative genomics, in vivo minigene analysis, datasets of homologous exons and introns

Lab contact: gilast@post.tau.ac.il

Lab website: http://www.tau.ac.il/~gilast/