Honey Bees and Malaria: Joseph DeRisi Presentation on Jan. 9
Jan. 4, 2012
DAVIS--Joseph DeRisi, a Howard Hughes Medical Institute investigator and professor and vice chair of the Department of Biochemistry and Biophysics at the University of California, San Francisco, will speak on two topics, honey bees and malaria, from 10 to 11 a.m. on Monday, Jan. 9, in the main auditorium (Room 2005) of the Genome and Biomedical Sciences Facilityon the UC Davis campus.
Joseph DeRisi (Photo courtesy of UC San Francisco)
His presentation, "A Seminar in Two Acts: Honey Bees and Malaria," is sponsored by the Biological Networks Focus Group of the Genome Center. Host is Oliver Fiehn, professor in the Department of Molecular and Cellular Biology and the Genome Center.
The Genome and Biomedical Sciences Facility is located at 451 Health Sciences Drive, the Health Sciences District, approximately 160 feet north of Tupper Hall.
DeRisi, a molecular biologist and biochemist, was named the recipient of a MacArthur Foundation Grant (also known as "the genius award") in 2004. In 2008, DeRisi won the Heinz Award for Technology, the Economy and Employment. Among his many accomplishments: he designed and programmed a groundbreaking tool for finding (and fighting) viruses -- the ViroChip, a DNA microarray that test for the presence of all known viruses in one step. (See link)
The DeRisi lab drew international attention last year with publications in Public Library of Science journals on malaria research (PLoS Biology) and honey bee research (PLoS One.)
Chemical Rescue of Malaria Parasites Lacking an Apicoplast Defines Organelle Function in Blood-Stage Plasmodium falciparum (published in PLoS Biology, August 2011)
Plasmodium spp. parasites harbor an unusual plastid organelle called the apicoplast. Due to its prokaryotic origin and essential function, the apicoplast is a key target for development of new anti-malarials. Over 500 proteins are predicted to localize to this organelle and several prokaryotic biochemical pathways have been annotated, yet the essential role of the apicoplast during human infection remains a mystery. Previous work showed that treatment with fosmidomycin, an inhibitor of non-mevalonate isoprenoid precursor biosynthesis in the apicoplast, inhibits the growth of blood-stage P.
falciparum. Herein, we demonstrate that fosmidomycin inhibition can be chemically rescued by supplementation with isopentenyl pyrophosphate (IPP), the pathway product. Surprisingly, IPP supplementation also completely reverses death following treatment with antibiotics that cause loss of the apicoplast. We show that antibiotic-treated parasites rescued with IPP over multiple cycles specifically lose their apicoplast genome and fail to process or localize organelle proteins,
rendering them functionally apicoplast-minus. Despite the loss of this essential organelle, these apicoplast-minus auxotrophs can be grown indefinitely in asexual blood stage culture but are entirely dependent on exogenous IPP for survival. These findings indicate that isoprenoid precursor biosynthesis is the only essential function of the apicoplast during blood-stage growth. Moreover, apicoplast-minus P. falciparum strains will be a powerful tool for further investigation of apicoplast biology as well as drug and vaccine development
Temporal Analysis of the Honey Bee Microbiome Reveals Four Novel Viruses and Seasonal Prevalence of Known Viruses, Nosema, and Crithidia (published in PLoS One, June, 2011)
Honey bees (Apis mellifera) play a critical role in global food production as pollinators of numerous crops. Recently, honey bee populations in the United States, Canada, and Europe have suffered an unexplained increase in annual losses due to a phenomenon known as Colony Collapse Disorder (CCD). Epidemiological analysis of CCD is confounded by a relative dearth of bee pathogen field studies. To identify what constitutes an abnormal pathophysiological condition in a honey bee colony, it is critical to have characterized the spectrum of exogenous infectious agents in healthy hives over time. We conducted a prospective study of a large scale migratory bee keeping operation using high-frequency sampling paired with comprehensive molecular detection methods, including a custom microarray, qPCR, and ultra deep sequencing. We established seasonal incidence and abundance of known viruses, Nosema sp., Crithidia mellificae, and bacteria. Ultra deep sequence analysis further identified four novel RNA viruses, two of which were the most abundant observed components of the honey bee microbiome (,1011 viruses per honey bee). Our results demonstrate episodic viral incidence and distinct pathogen patterns between summer and winter time-points. Peak infection of common honey bee viruses and Nosema occurred in the summer, whereas levels of the trypanosomatid Crithidia mellificae and Lake Sinai virus 2, a novel virus, peaked in January.
Among those working on the honey bee research and co-authoring the paper was insect virus researcher Michelle Flenniken, a postdoctoral fellow in the Raul Andino lab at UC San Francisco and the recipient of the Häagen-Dazs Postdoctoral Fellowship in Honey Bee Biology at UC Davis.
Among DeRisi's malaria research collaborators is UC Davis molecular biologist Shirley Luckhart, professor in the Department of Medical Microbiology and Immunology and an advisor in the Entomology Graduate Program.
DeRisi received a bachelor's degree in biochemistry and molecular biology in 1992 from the University of Santa Cruz, and his Ph.D. in biochemistry in 1999 from Stanford University.
Joseph DeRisi Lab, UC San Francisco
Joe DeRisi: Biochemist (featured in TED ("Technology, Entertainment, Design" is a nonprofit devoted to Ideas Worth Spreading.)
Conversation with Joe DeRisi (New York Times)
Solving Medical Mysteries (YouTube)
Hunting the Next Killer Virus (YouTube)
Joseph DeRisi: Howard Hughes Medical Institute
Joseph DeRisi in Wikipedia
--Kathy Keatley Garvey
UC Davis Department of Entomology