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Isolation and In vitro Activation of Caenorhabditis elegans Sperm
Published on: February 1, 2011
Stress-induced germ cell apoptosis by a p53 independent pathway in Caenorhabditis elegans
L S Salinas1, E Maldonado, R E Navarro
1Departamento de Biología Celular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apartado Postal 70-600, México, DF 04510, Mexico.
Abstract:
In Caenorhabditis elegans, several distinct apoptosis pathways have been characterized in the germline. The physiological pathway is though to eliminate excess germ cells during oogenesis to maintain gonad homeostasis and it is activated by unknown mechanisms. The DNA damage-induced germ cell apoptosis occurs in response to genotoxic agents and involves the proteins EGL-1 and CED-13, and the DNA damage response protein p53. Germ cell apoptosis can also be induced in response to pathogen infection through an EGL-1 dependent pathway. To gain insight into the mechanism and functions of germ cell apoptosis, we investigated whether and how other forms of stress induce this cell death. We found that oxidative, osmotic, heat shock and starvation stresses induce germ cell apoptosis through a p53 and EGL-1 independent pathway. We also learned that the MAPK kinases MEK-1 and SEK-1, and the p53 antagonist protein ABL-1, are essential for stress-induced germ cell apoptosis. We conclude that in C. elegans responses to various stresses that do not involve genotoxicity include an increase in germ cell apoptosis through the physiological pathway.
Insights
Oxidative, osmotic, heat shock, and starvation stresses trigger germ cell apoptosis in C. elegans via a pathway independent of p53 and EGL-1, involving MEK-1, SEK-1, and ABL-1.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Apoptosis in the C. elegans germline eliminates excess germ cells for gonad homeostasis.
- Known pathways include physiological, DNA damage-induced (p53, EGL-1, CED-13), and pathogen-induced (EGL-1) apoptosis.
Purpose of the Study:
- To investigate if and how non-genotoxic stresses induce germ cell apoptosis.
- To elucidate the molecular mechanisms underlying stress-induced germ cell apoptosis.
Main Methods:
- Induction of germ cell apoptosis using various stresses (oxidative, osmotic, heat shock, starvation) in C. elegans.
- Genetic analysis utilizing mutants for key apoptosis regulators (p53, EGL-1) and signaling molecules (MEK-1, SEK-1, ABL-1).
Main Results:
- Oxidative, osmotic, heat shock, and starvation stresses induce germ cell apoptosis.
- This stress-induced apoptosis is independent of p53 and EGL-1.
- MAPK kinases MEK-1 and SEK-1, and the p53 antagonist ABL-1, are essential for this process.
Conclusions:
- C. elegans germ cell apoptosis can be triggered by various stresses that do not involve genotoxicity.
- These stresses activate the physiological apoptosis pathway through novel molecular players.
- The findings reveal a distinct stress response pathway in germ cell death regulation.
