Research Interests:
Hypertension and chromaffin cell research at UCSD.
Questions.
Each of us has a genome of increasingly well-defined sequence of ~3.3 Mbp. And each of us differs from one another in a host of traits (phenotypes), ranging from physical appearance to disease. But to what extent does common genetic variation in the population determine our traits, and especially our predisposition to disease? And what are the relative roles of heredity and environment ("nature versus nurture") in trait determination?
Approaches.
Our lab works on genetic determination of common, complex human cardiovascular/renal traits, such as hypertension, renal function/disease, heritable responses to environmental stress, and antihypertensive drug responses. Our work employs several complementary disciplines, amounting to a "toolbox": Phenotyping of
human twin pairs and pedigrees [which help us to tease out the relative roles of heredity and environment on trait determination];Population genetics; Genome technology (DNA sequencing for polymorphism discovery and typing); informatics (relational databasing of phenotypic and genomic information); Statistical genetics (mapping genetic variation onto phenotypic variance); Bioinformatics (understanding the predicted significance of genetic variation); and Molecular/cell biology (experimentally determining whether genetic variants alter function of either transcriptional units or open reading frames, usually in chromaffin cells).
This may sound like quite a mouthful, but these are essential and complementary elements in the quest to determine how genetic variation influences such complex traits as hypertension.
Track(s):
Molecular Pharmacology
Genetics
|
News