Fungal Genomics & Biology

Fungal Genomics & Biology
Open Access

ISSN: 2165-8056

Martin Kupiec

Martin Kupiec

President, Genetic Society of Israel

He completed B.Sc. from Hebrew University, Jerusalem,in 1978 & PhD. Hebrew University, Jerusalem, Genetics in 1985.
Research Interest

The Kupiec laboratory uses “the awesome power of yeast genetics” to investigate basic universal processes that are very hard to study in other organisms. Our basic methodology involves Molecular Biology techniques. As yeast is today the best understood eukaryotic organism, with more than half of its genes with a known function/activity, the new genetic and molecular tools developed in yeast have jump-started a REVOLUTION IN BIOLOGY: Systems Biology. We are able, for the first time, to ask very basic questions about the way genomes are organized, genes interact, proteins talk to each other, etc. This genome-wide approach requires novel tools, which we are helping to develop in cooperation with people from Computer Science at TAU. Most of the essential pathways, complexes and genes involved in basic cellular processes are conserved in evolution, and human orthologs are present for most of the genes we study. Here are some of the basic biological questions that we are trying to understand, using the baker’s yeast (Saccharomyces cerevisiae) and fission yeast (Schizosaccharomyces pombe) as a model organisms: DNA repair: Our cells are constantly exposed to radiation and chemicals that cause damage to the DNA or even break the chromosomes in pieces. Even natural cellular metabolism creates oxidative stress and DNA damage. Luckily we have efficient mechanisms to repair the damage. Stability of the eukaryotic genome: Normal cells have remarkably stable karyotypes. You can easily identify to what species a cell belongs, just by looking at its chromosomes. However, cancer cells lose this stability, and start accumulating translocations, deletions, amplifications, etc. Many of the endpoints of these rearrangements fall in repeated sequences (sometimes called “junk DNA”) that fill-up our genomes. What prevents a high level of chromosomal aberrations as a consequence of recombination between repeated sequences? Telomeres: Telomeres are nucleoprotein complexes at the end of the eukaryotic chromosomes. We would like to know how do all these genes work together to regulate telomere length. Are there several pathways? Complexes? What are the interactions between the various elements? To answer these questions we are using a combination of Molecular Biology, Systems Biology, Genetics and Biochemistry. Bioinformatic models are used as a basis to plan possible experiments. The results are then incorporated into the model, to generate more predictions in a continuous cycle that progressively refines the model. The TOR protein kinase: The TOR protein kinases exhibit a conserved role in regulating cellular growth and proliferation. We would like to answer some of the following questions: What is the function of each of the Tor proteins? What is the nature of their interactions? How are they regulated? Why are mammalian cells and budding yeast so affected by rapamycin (an anticancer drug in clinical trials), whereas fission yeast can grow in its presence? How do the Tor proteins integrate signals from the environment to know when to grow? And how do they talk to the cell cycle machinery to coordinate growth (in volume) with cell division?

Relevant Topics