J Tesarik1. 1. Laboratoire d'Eylau, Paris, France.
Abstract
PURPOSE: Cell cycle-related calcium signals, bearing some similarity to those previously described in other animal species, have also been observed in human preimplantation embryos. These signals follow those occurring in both gametes during the period preceding fertilization and those induced by the fertilizing spermatozoon in the oocyte after gamete fusion. Even though the signals occurring during each of these distinct developmental periods have different temporal and spatial characteristics, there may be a relationship between them; in fact, abnormalities of calcium signals occurring in an earlier developmental period may be at the origin of abnormal signals during later developmental periods. METHODS: Possible mechanisms by which inadequate or truncated calcium signals can impair embryo development are discussed. RESULTS: These mechanisms include complete failure of the second meiotic division, leading to triploidy; incomplete failure of the second meiotic division, leading to de novo chromosomal numerical abnormalities; abnormal pronuclear development and function; abnormalities of the blastomere cell cycle, possibly leading to embryo cleavage arrest, and problems with blastomere allocation to embryonic cell lineages, leading to disproportionate development of the inner cell mass and trophectoderm derivatives, which can be the origin of implantation failure or miscarriage. CONCLUSIONS: Future research should make it possible to decipher the nature of normal development signals, to determine the key checkpoints at which these signals are required to prevent the switch to apoptosis, and to examine the possibilities of therapeutic action at these checkpoints to rescue the endangered embryo for normal development.
PURPOSE: Cell cycle-related calcium signals, bearing some similarity to those previously described in other animal species, have also been observed in human preimplantation embryos. These signals follow those occurring in both gametes during the period preceding fertilization and those induced by the fertilizing spermatozoon in the oocyte after gamete fusion. Even though the signals occurring during each of these distinct developmental periods have different temporal and spatial characteristics, there may be a relationship between them; in fact, abnormalities of calcium signals occurring in an earlier developmental period may be at the origin of abnormal signals during later developmental periods. METHODS: Possible mechanisms by which inadequate or truncated calcium signals can impair embryo development are discussed. RESULTS: These mechanisms include complete failure of the second meiotic division, leading to triploidy; incomplete failure of the second meiotic division, leading to de novo chromosomal numerical abnormalities; abnormal pronuclear development and function; abnormalities of the blastomere cell cycle, possibly leading to embryo cleavage arrest, and problems with blastomere allocation to embryonic cell lineages, leading to disproportionate development of the inner cell mass and trophectoderm derivatives, which can be the origin of implantation failure or miscarriage. CONCLUSIONS: Future research should make it possible to decipher the nature of normal development signals, to determine the key checkpoints at which these signals are required to prevent the switch to apoptosis, and to examine the possibilities of therapeutic action at these checkpoints to rescue the endangered embryo for normal development.