Subcellular dynamics of the maternal cell death regulator BCL2L10 in human preimplantation embryos

What is the expression status and subcellular localization of the maternally expressed Bcl-2 family member, BCL2L10, in early human embryos of diverse developmental stages and quality? The anti-apoptotic protein, BCL2L10, is expressed in human preimplantation embryos at least until the blastocyst stage and appears to be differentially distributed at the subcellular level between viable embryos and fragmented or arrested embryos. BCL2L10 is an anti-apoptotic member of the BCL-2 family that shows abundant expression in human oocytes and limited sequence conservation to its mouse homologue. Embryos donated with informed consent by couples consulting for infertility in the Department of Reproductive Medicine (Hpital Femme Mre Enfant, Bron, France) were divided into two groups: high quality embryos (n 18) and poor quality embryos (n 30). Semen samples (n 4) were obtained after informed consent from men consulting for couple infertility. Experiments involving human preimplantation embryos were performed between January and December 2009. We examined BCL2L10 expression and subcellular localization in early human embryos by using immunofluorescence and confocal microscopy. The subcellular distribution of BCL2L10 was also studied in ejaculated sperm cells and in isolated mouse skeletal muscle fibres. The BCL2L10 protein was detectable in healthy human preimplantation embryos at least until the blastocyst stage. In high-quality embryos, BCL2L10 was predominantly cytoplasmic with mitochondrial localization. In contrast, BCL2L10 exhibited extra-mitochondrial localization in abnormal embryos, and was nuclearcytoplasmic in approximately half (17/30) of the poor-quality embryos. Morphologically fragmented embryos showed coexistence of blastomeres with BCL2L10-positive expression and blastomeres or fragments negative for BCL2L10. Future studies are needed to evaluate whether embryo quality is related to an exclusive mitochondrial localization of BCL2L10. Mechanisms mediating the nuclear translocation of BCL2L10 in abnormal embryos and functions of this nuclear pool of BCL2L10 are currently unknown. The nuclear localization of BCL2L10 in abnormal embryos suggests a potential role for this protein in pathological conditions resulting in embryo arrest. No external funding was obtained for this study. There are no competing interests.