Affiliation: UCSD SOM
Professor of Pathology
1963 B.S., Carnegie-Mellon University, Pittsburgh, PA (Honors
1967 Ph.D. Case Western Reserve Univ., Cleveland, OH, NIH Pre-doctoral
Postdoctoral Fellow: Dept. of Genetics, Stanford University,
National Institutes of Health
Professor of Pathology, Division of Infectious Diseases, UCSD
Member, Center for Molecular Genetics
Giardia is a major cause of waterborne intestinal disease and
is also of basic biological interest as one of the earliest known
eukaryotic organisms, with both prokaryotic and eukaryotic properties.
Our group's orientation is unusual because we focus broadly on
this organism and are not tied to specific techniques (Ann. Rev.
Microbiol. 50: 679-705,1996). Our lab has completed the giardial
life cycle in vitro for the first time, by inducing the flagellated
"trophozoite" form that colonizes the small intestine to differentiate
into cysts that survive in the environment. We discovered a novel
regulated secretory pathway for the transport of cyst wall proteins
during encystation. Cysts infect a new host by responding to signals
from the host that lead to a rapid and dramatic differentiation.
Excystation entails establishing cellular polarity, cell division,
attachment, increases in metabolism, and antigenic switching.
Current questions include:
1. How are giardial genes regulated during differentiation?
2. What are the cell signaling pathways in differentiation and
3. What is the nature of giardial "crosstalk" with the host'
4. What are the structure and function of the unusual cysteine-rich
variant surface protein of Giardia?
5. What can Giardial genes and pathways tell us about the evolution
of the eukaryotic cell?
6. How does Giardia make people sick?
References From PubMed (NCBI)