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Published on: January 1, 2018
Baculovirus p35 prevents developmentally programmed cell death and rescues a ced-9 mutant in the nematode
A Sugimoto1, P D Friesen, J H Rothman
1Department of Biochemistry, University of Wisconsin-Madison 53706.
Abstract:
Programmed cell death, or apoptosis, occurs throughout the course of normal development in most animals and can also be elicited by a number of stimuli such as growth factor deprivation and viral infection. Certain morphological and biochemical characteristics of programmed cell death are similar among different tissues and species. During development of the nematode Caenorhabditis elegans, a single genetic pathway promotes the death of selected cells in a lineally fixed pattern. This pathway appears to be conserved among animal species. The baculovirus p35-encoding gene (p35) is an inhibitor of virus-induced apoptosis in insect cells. Here we demonstrate that expression of p35 in C. elegans prevents death of cells normally programmed to die. This suppression of developmentally programmed cell death results in appearance of extra surviving cells. Expression of p35 can rescue the embryonic lethality of a mutation in ced-9, an endogenous gene homologous to the mammalian apoptotic suppressor bcl-2, whose absence leads to ectopic cell deaths. These results support the hypothesis that viral infection can activate the same cell death pathway as is used during normal development and suggest that baculovirus p35 may act downstream or independently of ced-9 in this pathway.
Insights
The baculovirus p35 gene inhibits programmed cell death (apoptosis) in C. elegans, preventing normal cell death and rescuing mutations. This suggests viral apoptosis pathways overlap with developmental ones.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Programmed cell death, or apoptosis, is crucial for animal development and can be triggered by various stimuli.
- The nematode Caenorhabditis elegans utilizes a conserved genetic pathway for programmed cell death during development.
- Baculovirus p35 is known to inhibit apoptosis in insect cells.
Purpose of the Study:
- To investigate the role of baculovirus p35 in regulating programmed cell death during C. elegans development.
- To determine if p35 can suppress developmentally programmed cell death and its interaction with endogenous apoptotic regulators.
Main Methods:
- Expression of baculovirus p35 in C. elegans.
- Analysis of cell survival and embryonic lethality in transgenic and mutant strains.
- Investigating the genetic interaction between p35 and the ced-9 gene.
Main Results:
- Expression of p35 in C. elegans prevented the normal death of developmentally programmed cells, leading to the survival of extra cells.
- p35 expression rescued embryonic lethality caused by mutations in ced-9, a gene homologous to bcl-2.
- These findings indicate that p35 acts on the apoptotic pathway.
Conclusions:
- Baculovirus p35 effectively suppresses developmentally programmed cell death in C. elegans.
- The results support the hypothesis that viral apoptosis pathways are conserved and can utilize similar mechanisms as developmental pathways.
- p35 may function downstream or independently of the ced-9 gene in the apoptotic pathway.
