Subcellular dynamics of the maternal cell death regulator BCL2L10 in human preimplantation embryos.
Human Reproduction. 2013-01-04; 28(3): 729-739
DOI: 10.1093/humrep/des443
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Guérin JF(1), Cornut-Thibaut A, Giscard-Destaing S, Pouvreau S, Guillemin Y,
Aouacheria A.
Author information:
(1)Service de Médecine de la Reproduction, Hôpital Femme-Mère-Enfant, Bron
F-69500, France.
STUDY QUESTION: 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?
SUMMARY ANSWER: 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.
WHAT IS KNOWN ALREADY: 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.
STUDY DESIGN, SIZE, DURATION: Embryos donated with informed consent by couples
consulting for infertility in the Department of Reproductive Medicine (Hôpital
Femme Mère 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.
PARTICIPANTS/MATERIALS, SETTING, METHODS: 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.
MAIN RESULTS AND THE ROLE OF CHANCE: 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 nuclear-cytoplasmic 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.
LIMITATIONS, REASONS FOR CAUTION: 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.
WIDER IMPLICATIONS OF THE FINDINGS: The nuclear localization of BCL2L10 in
abnormal embryos suggests a potential role for this protein in pathological
conditions resulting in embryo arrest.
STUDY FUNDING/COMPETING INTEREST(S): No external funding was obtained for this
study. There are no competing interests.
DOI: 10.1093/humrep/des443
PMID: 23293224 [Indexed for MEDLINE]