In all mammalian species studied, a marked oocyte loss occurs during the fetal life before their enclosure within the primordial follicle. The concept that female mammals are born with all of the oocytes they will ever posses and the consequent notion that the age-related ovarian failure and menopause occur when the oocyte ovarian reserve is exhausted, render particular relevant to understand the reasons and the mechanisms of oocyte demise in the fetal ovary. Over the years, three main hypotheses to explain the cause of fetal oocyte death have been proposed: 1) the number of oocytes formed in the ovary is in excess respect to the supporting cell, 2) the process of cross over central in prophase I, requires critical molecular processes subjected to frequent errors leading to oocyte death and 3) most oocytes could sacrify themselves donating their cytoplasm content to a subset of surviving oocytes. Mainly during the last three decades, researchers have reported evidence favoring each of these hypotheses; thus suggesting that the survival or death of fetal oocytes depends on several conditions and mechanisms. The concept that cell death is a carefully controlled process both at genomic and molecular level termed apoptosis or programmed cell death (PCD) affirming at the beginning of eighty years, stimulated researchers to analyze in more details the morphological and molecular characteristics as well as the kinetics of the fetal oocyte elimination. In the next sections of the present chapter, we will critically review the principal studies carried out, mainly in the mouse, in our and other laboratories that are slowly disclosing the complexity of the fetal oocyte elimination.

Klinger, F.g., DE FELICI, M. (2011). Programmed cell death in fetal oocytes. In G.H. Vázquez-Nin, M.L. Escobar, M. De Felici, O.M. Echeverría, F.G. Klinger (a cura di), Cell death in the mammalian ovary (pp. 125-142). Springer [10.1007/978-94-007-1134-1_8].

Programmed cell death in fetal oocytes

KLINGER, FRANCESCA GIOIA;DE FELICI, MASSIMO
2011-01-01

Abstract

In all mammalian species studied, a marked oocyte loss occurs during the fetal life before their enclosure within the primordial follicle. The concept that female mammals are born with all of the oocytes they will ever posses and the consequent notion that the age-related ovarian failure and menopause occur when the oocyte ovarian reserve is exhausted, render particular relevant to understand the reasons and the mechanisms of oocyte demise in the fetal ovary. Over the years, three main hypotheses to explain the cause of fetal oocyte death have been proposed: 1) the number of oocytes formed in the ovary is in excess respect to the supporting cell, 2) the process of cross over central in prophase I, requires critical molecular processes subjected to frequent errors leading to oocyte death and 3) most oocytes could sacrify themselves donating their cytoplasm content to a subset of surviving oocytes. Mainly during the last three decades, researchers have reported evidence favoring each of these hypotheses; thus suggesting that the survival or death of fetal oocytes depends on several conditions and mechanisms. The concept that cell death is a carefully controlled process both at genomic and molecular level termed apoptosis or programmed cell death (PCD) affirming at the beginning of eighty years, stimulated researchers to analyze in more details the morphological and molecular characteristics as well as the kinetics of the fetal oocyte elimination. In the next sections of the present chapter, we will critically review the principal studies carried out, mainly in the mouse, in our and other laboratories that are slowly disclosing the complexity of the fetal oocyte elimination.
2011
Settore BIO/17 - ISTOLOGIA
English
Rilevanza internazionale
Capitolo o saggio
apoptosis; oocytes; fetal ovary; oogenesis; reproduction; germ cells
Klinger, F.g., DE FELICI, M. (2011). Programmed cell death in fetal oocytes. In G.H. Vázquez-Nin, M.L. Escobar, M. De Felici, O.M. Echeverría, F.G. Klinger (a cura di), Cell death in the mammalian ovary (pp. 125-142). Springer [10.1007/978-94-007-1134-1_8].
Klinger, Fg; DE FELICI, M
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/22212
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