Purpose: Cell cycle-related calcium signals, bearing some similarity to tho
se previously described in other animal species, have also been observed in
human preimplantation embryos. These signals follow those occurring in bot
h gametes during the period preceding fertilization and those induced by th
e fertilizing spermatozoon in the oocyte after gamete fusion. Even though t
he signals occurring during each of these distinct developmental periods ha
ve different temporal and spatial characteristics, there may be a relations
hip between them; in fact, abnormalities of calcium signals occurring in an
earlier developmental period may be at the origin of abnormal signals duri
ng later developmental periods.
Methods: Possible mechanisms by which inadequate or truncated calcium signa
ls call impair embryo development are discussed.
Results: These mechanisms include complete failure of the second meiotic di
vision, leading to triploidy; incomplete failure of the second meiotic divi
sion, leading to de novo chromosomal numerical abnormalities; abnormal pron
uclear 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 developm
ent 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 developmental signals, to determine the key checkpoints at which
these signals are required to prevent the switch to apoptosis, and to exam
ine the possibilities of therapeutic action at these checkpoints to rescue
the endangered embryo for normal development.