Caspase-2 deficiency prevents programmed germ cell death resulting from cytokine insufficiency but not meiotic defects caused by loss of ataxia telangiectasia-mutated (Atm) gene function

Citation
Y. Morita et al., Caspase-2 deficiency prevents programmed germ cell death resulting from cytokine insufficiency but not meiotic defects caused by loss of ataxia telangiectasia-mutated (Atm) gene function, CELL DEAT D, 8(6), 2001, pp. 614-620
Citations number
61
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL DEATH AND DIFFERENTIATION
ISSN journal
1350-9047 → ACNP
Volume
8
Issue
6
Year of publication
2001
Pages
614 - 620
Database
ISI
SICI code
1350-9047(200106)8:6<614:CDPPGC>2.0.ZU;2-S
Abstract
It is well established that programmed cell death claims up to two-thirds o f the oocytes produced during gametogenesis in the developing fetal ovaries , However, the mechanisms underlying prenatal germ cell loss in females rem ain poorly understood, Herein we report that caspase-11 null female mice ar e born with a reduced number of oocyte-containing primordial follicles, Thi s phenotype is likely due to failed cytokine processing known to occur in c aspase-11 mutants since neonatal female mice lacking both interleukin (IL)- 1 alpha and IL-1 beta also exhibit a reduced endowment of primordial follic les, In addition, germ cell death in wild-type fetal ovaries cultured ex vi vo is suppressed by either cytokine, likely via ligand activation of type 1 IL-1 receptors expressed in fetal germ cells, Normal oocyte endowment can be restored in caspase-11 null female mice by simultaneous inactivation of the gene encoding the cell death executioner enzyme, caspase-2, However, ca spase-2 deficiency cannot overcome gametogenic failure resulting from meiot ic recombination defects in ataxia telangiectasia-mutated (Atm) null female mice, Thus, genetically distinct mechanisms exist for developmental deleti on of oocytes via programmed cell death, one of which probably functions as a meiotic quality-control checkpoint that cannot be overridden.