John Boothroyd
Department of Microbiology and Immunology
Stanford University School of Medicine

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John Boothroyd, Ph.D.
Professor and Chair
Dept. of Microbiology & Immunology
Fairchild Building D305
Stanford University School of Medicine
Stanford, CA 94305-5124 Tel: (650) 723-7984; FAX: (650) 723-6853
email: John.Boothroyd@Stanford.edu
Studies on the cell and molecular biology of parasitic protozoa are critically important for two reasons. First, these organisms are pathogens of devastating magnitude, particularly in developing countries. Second, they have proven to be a source of many remarkable phenomena some of which have ultimately been found to be present in many eukaryotes (e.g., GPI anchors, trans-splicing, etc.) and some of which are so far unique (e.g., RNA editing and kinetoplast DNA). We are putting all of our current effort into studies of the obligate intracellular parasite, Toxoplasma gondii. This is a member of the Apicomplexa which includes the causative agent of malaria and coccidiosis. This group of parasites is named for an extraordinary complex of apical organelles dedicated to invasion of the host cell.
Toxoplasma is perhaps the most wide-spread parasite on earth with infection being possible in almost any warm-blooded animal and with prevalence rates in many regions being extremely high (e.g., ~75% of adult humans in France are infected). The parasite has a complex life cycle which includes two sub-cycles: a sexual cycle, complete with male and female gametes and production of environmentally robust oocysts shed in the feces (for some reason, this occurs only in cats) and an asexual cycle in all hosts.

Our interests are in the novel aspects of Toxoplasma biology. Specifically:
(i) how does Toxoplasma attach to and invade almost any eukaryotic cell it encounters? [the surface and complex apical structures are clearly key to thiese processes].
(ii) how does the parasite nurture itself within the parasitophorous vacuole it creates inside the host cell? [the mitochondrion and plastid organelles appear key here.]
(iii) how does Toxoplasma evade the immune response of the host? [the diverse but related surface antigens may be modulating the immune response.]
(iv) how are proteins destined for novel organelles specifically targeted? [Toxoplasma has two unusual secretory compartments, the rhoptries and micronemes, as well as more traditional structures like dense granules, all with distinct contents that must be appropriately targeted.] sec
(v) what are the signals and mechanisms that control gene expression during development from the chronic "bradyzoite" form to the active "tachyzoite" stage? [evidence exists for both transcriptional and post-transcriptional control mechanisms.]
(vi) what are the physiological differences between these two developmental forms? [here, EST analysis and promoter-trap studies are revealing several unusual pathways.]
(vii) what are the real mechanisms by which anti-toxoplasma drugs that are currently in clinical use function? [of special interest are the antibiotic clindamycin and a product used for both Plasmodium and Toxoplasma known as atovaquone.]
For more detailed information, you can visit the Boothroyd Lab Home Page.

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