People
Nancy Beckage
Mailing Address:
EntomologyEntomology /382
University of California
Riverside, CA 92521
Phone: (951) 827-3521
Fax: (951) 827-3087
Email: nancy.beckage@ucr.edu
Degree(s):
PhD 1980 University of WisconsinBS 1980 University of Wisconsin
College/Division Affiliation:
College of Natural and Agricultural SciencesCenter/Inst Affiliation(s):
Center for Disease Vector ResearchBiotechnology Impacts Center
Areas Of Expertise:
Physiological and Molecular Host-parasite Relationships; Insect Immunity, Pathology, Virology, Endocrinology, and Behavior; Vector Biology, Physiology, and Vector-parasite Interactions; Host-parasitoid InteractionsAwards / Honors:
2005 Chancellor's Faculty Award for Excellence in Mentorship of Undergraduate Research2003 AAAS Fellow (American Association for the Advancement of Science)
1996 UC Riverside "Women Who Make a Difference Award"
1996 Miller Visiting Research Professor, University of California Berkeley
1992 Distinguished Lectureship, Montana State University - Molecular Biology
1975-79 National Institutes of Health Developmental Biology Predoctoral Fellowship
Research Summary:
My laboratory has focused its efforts in deciphering the complexities of biochemical and molecular host-pathogen and hostparasite relationships, with special emphasis on wasp parasitoids that kill their hosts. The wasp parasitoid Cotesia congregata injects a polydnavirus (polydisperse DNA virus) into its host, the tobacco hormworm (Manduca sexta). The wasp genome contains integrated viral sequences, and the viruses replicate only in the female wasp's ovarian calyx tissue. The viruses cause host immunosuppression (the equivalent of an insect AIDS-like virus), allowing the parasitoids to mature without invoking a host immune response. The polydnavirus triggers apoptosis of host hemocytes, thus causing the host to be immunosuppressed during the initial stages of parasitic infection. Integration of viral sequences in the genomic DNA of the wasp itself is under study. Future studies are being directed at deciphering the role of virus-encoded proteins in causing host immunosuppression. Another area of special interest concerns the role of the parasitoid's polydnavirus in the successful interaction between the parasites and their host via expression of PDV gene products. A major hemolymph protein is induced to appear in the host beginning immediately following parasitization and this protein is a polydnavirus transcript. Host hemocytes, fat body, and other tissues participate in its synthesis to varying degrees. Viral DNAs persist in the host for the duration of parasitism. We are now exploring the biological role of the protein in causing host immunosuppression and other physiological changes. Endocrine relationships between the partners also are being examined, with particular emphasis on mechanisms of host developmental arrest involving endocrine and neuroendocrine disruption. Parasitized larvae show enhanced accumulation of neuropeptides in neurosecretory cells of the endocrine system. Hundreds of species of wasp parasitoids cause a similar host arrest, hence their utility as biological control agents. A common mechanism, such as disruption of neuropeptide release, may account for many species' ability to cause developmental arrest of their host insect in a pre-metamorphic state. The hemolymph ecdysteroid titer of the host peaks shortly before the wasps emerge. Wasp endo- and ectoparasitoids clearly have evolved the capacity to interact with their host via a variety of complex hormonal and biochemical interactions. This is particularly true of parsitoids that ultimately induce developmental arrest and cause death of the host. Behavioral effects of parasitism are also seen.Selected Publications:
Lab Personnel: +
- Cathers, Cathy
- Graduate Student — Ecdysone agonist insect growth regulators as mosquito biopesticides
- MacWilliam, Dyan
- Graduate Student — Neural regulation of insect host behaviors during parasitism