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Expression of baculovirus P35 prevents cell death in Drosophila
1Howard Hughes Medical Institute, University of California Berkeley 94720-3200.
Abstract:
The baculovirus P35 protein functions to prevent apoptotic death of infected cells. We have expressed P35 in the developing embryo and eye of the fly Drosophila melanogaster. P35 eliminates most, if not all, normally occurring cell death in these tissues, as well as X-irradiation-induced death. Excess pupal eye cells that are normally eliminated by apoptosis develop into pigment cells when their death is prevented by P35 expression. Our results suggest that one mechanism by which viruses prevent the death of the host cell is to block a cell death pathway that mediates normally occurring cell death. Identification of molecules that interact biochemically or genetically with P35 in Drosophila should provide important insights into how cell death is regulated.
Insights
The baculovirus P35 protein prevents programmed cell death in Drosophila melanogaster. This finding suggests viruses block host cell death pathways, offering insights into cell death regulation.
Area of Science:
- Molecular Biology
- Developmental Biology
- Virology
Background:
- Baculovirus P35 protein inhibits apoptosis in infected cells.
- Apoptosis, or programmed cell death, is crucial for normal development and tissue homeostasis.
- Understanding cell death regulation is vital in biology and disease.
Purpose of the Study:
- To investigate the function of baculovirus P35 protein in a multicellular organism.
- To determine if P35 can inhibit developmentally regulated and stress-induced cell death.
- To explore the role of P35 in cell fate determination during development.
Main Methods:
- Expression of baculovirus P35 protein in Drosophila melanogaster embryos and eyes.
- Analysis of cell death in P35-expressing tissues using normal development and X-irradiation as stimuli.
- Observation of cell fate changes in response to inhibited apoptosis.
Main Results:
- P35 expression significantly reduced or eliminated normal developmental cell death in Drosophila tissues.
- P35 also prevented X-irradiation-induced cell death.
- Inhibition of apoptosis in pupal eyes led to the transformation of excess cells into pigment cells.
Conclusions:
- Viruses may prevent host cell death by targeting conserved cell death pathways.
- The P35 protein interferes with endogenous cell death mechanisms.
- Drosophila serves as a valuable model for studying cell death regulation and identifying interacting molecules.