Interactome networks and human disease

Published on December 2, 2014   39 min

Other Talks in the Series: Systems Biology

My name is Marc Vidal. I'm the Founding Director of the Center for Cancer Systems Biology at the Dana-Farber Cancer Institute and Professor of Genetics at Harvard Medical School. This presentation will discuss the notion of interactome networks. We will explore how complex networks of interacting macromolecules, or so-called interactome networks, might underlie biological functions. And we will summarize recent findings that describe how perturbations of interactive networks might relate to human disease.
One of the major goals of Biology is to understand the mechanisms that underlie genotype-phenotype relationships. How do Mendelian mutations lead to Mendelian disorders? How do functional variants located in loci found in Genome-Wide Association Studies, or GWAS, lead to complex traits? And how do cancer-associated mutations lead to tumorigenesis? These are questions for which we still lack mechanistic answers in many cases.
One set of models to explain genotype-phenotype relationships is based on linear cause and effects relationships, according to which it is relatively convenient to directly associate a single genotypic variation to a single phenotypic manifestation.
These models originated from a very powerful and profound idea that launched the molecular biology revolution of the 20th century from Mendel to the DNA double helix which states that there are relatively simple relationships between genes, their products and the function these products mediate in the cell. Particularly, Beadle and Tatum, in their famous paper entitled, "Genetic Control of Biochemical Reactions in Neurospora" stated that the inability of neurospora mutants to synthesize vitamin B6 is apparently differentiated by a single gene. This simplifying concept literally revolutionized our understanding of genotype-phenotype relationships, but does it apply to all situations?