title: Stress-induced germ cell apoptosis by a p53 independent pathway in Caenorhabditis elegans.
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.
authors.affiliation: Departamento de Biología Celular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apartado Postal 70-600, México, DF 04510, Mexico.
authors.forename: L S
authors.initials: LS
authors.lastname: Salinas
authors.forename: E
authors.initials: E
authors.lastname: Maldonado
authors.forename: R E
authors.initials: RE
authors.lastname: Navarro
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D017173:Caenorhabditis elegans / Q000166:cytology / Q000235:genetics / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000502:physiology; D004249:DNA Damage / Q000235:genetics / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation; D005854:Germ Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D018882:Heat Stress Disorders / Q000235:genetics / Q000503:physiopathology; D006540:Herbicides / Q000494:pharmacology; D048369:MAP Kinase Kinase 1 / Q000235:genetics / Q000502:physiology; D048670:MAP Kinase Kinase 4 / Q000235:genetics / Q000502:physiology; D009866:Oogenesis / Q000235:genetics / Q000502:physiology; D009997:Osmotic Pressure; D018384:Oxidative Stress / Q000235:genetics / Q000502:physiology*; D010269:Paraquat / Q000494:pharmacology; D016315:Proto-Oncogene Proteins c-abl / Q000235:genetics / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology*
chemical_list: C438244:CEP-1 protein, C elegans; D029742:Caenorhabditis elegans Proteins; C504038:Ced-13 protein, C elegans; C112486:EGL-1 protein, C elegans; D006540:Herbicides; D017382:Reactive Oxygen Species; D012097:Repressor Proteins; D016159:Tumor Suppressor Protein p53; C516680:ABL-1 protein, C elegans; D016315:Proto-Oncogene Proteins c-abl; D048369:MAP Kinase Kinase 1; D048670:MAP Kinase Kinase 4; C516678:mek-1 protein, C elegans; C516679:sek-1 protein, C elegans; D010269:Paraquat