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0:00
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.
0:39
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.
1:14
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.
1:35
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?
