“…The mouse zygotic genome is transcriptionally activated soon after the first embryo cleavage (15,20,23). Two additional mitotic divisions then lead the embryo to the 8-cell stage at which its peripheral blastomeres compact and establish tight and gap junctional communications with each other (21,24), eventually resulting in blastocoel cavity formation. Our results indicate that Tcl1-deficient embryos acquire major differentiative traits normally and with the appropriate developmental timing.…”
Overexpression of the TCL1 oncogene has been shown to play a causative role in T cell leukemias of humans and mice. The characterization of Tcl1-deficient mice in these studies indicates an important developmental role for Tcl1 in early embryogenesis. In wild-type embryos, Tcl1 is abundant in the first three mitotic cycles, during which it shuttles between nuclei and the embryo cortical regions in a cell-cycle-dependent fashion. The absence of this protein in early embryogenesis results in reduced fertility of female mice. The present studies elucidate the mechanism responsible for the reduced female fertility through analysis of the oogenesis stages and early embryo development in Tcl1-deficient mice. Even though Tcl1 ؊/؊ females display normal oogenesis and rates of oocyte maturation͞ovulation and fertilization, the lack of maternally derived Tcl1 impairs the embryo's ability to undergo normal cleavage and develop to the morula stage, especially under in vitro culture conditions. Beyond this crisis point, differentiative traits of zygotic genome activation and embryo compaction can take place normally. In contrast with this unanticipated role in early embryogenesis, we observed an overexpression of TCL1 in human seminomas. This finding suggests that TCL1 dysregulation could contribute to the development of this germinal cell cancer as well as lymphoid malignancies.
“…The mouse zygotic genome is transcriptionally activated soon after the first embryo cleavage (15,20,23). Two additional mitotic divisions then lead the embryo to the 8-cell stage at which its peripheral blastomeres compact and establish tight and gap junctional communications with each other (21,24), eventually resulting in blastocoel cavity formation. Our results indicate that Tcl1-deficient embryos acquire major differentiative traits normally and with the appropriate developmental timing.…”
Overexpression of the TCL1 oncogene has been shown to play a causative role in T cell leukemias of humans and mice. The characterization of Tcl1-deficient mice in these studies indicates an important developmental role for Tcl1 in early embryogenesis. In wild-type embryos, Tcl1 is abundant in the first three mitotic cycles, during which it shuttles between nuclei and the embryo cortical regions in a cell-cycle-dependent fashion. The absence of this protein in early embryogenesis results in reduced fertility of female mice. The present studies elucidate the mechanism responsible for the reduced female fertility through analysis of the oogenesis stages and early embryo development in Tcl1-deficient mice. Even though Tcl1 ؊/؊ females display normal oogenesis and rates of oocyte maturation͞ovulation and fertilization, the lack of maternally derived Tcl1 impairs the embryo's ability to undergo normal cleavage and develop to the morula stage, especially under in vitro culture conditions. Beyond this crisis point, differentiative traits of zygotic genome activation and embryo compaction can take place normally. In contrast with this unanticipated role in early embryogenesis, we observed an overexpression of TCL1 in human seminomas. This finding suggests that TCL1 dysregulation could contribute to the development of this germinal cell cancer as well as lymphoid malignancies.
“…Reports from Capco (1999, 2000) have shown a marked reduction in the nuclear localization of these isotypes after the two-cell stage with the exception that PKC lines the nuclear periphery at the four-cell stage. However, these isotypes appear in unique locations poised to presumably interact during subsequent developmental transitions: At the time of compaction PKC , , , and µ line the cell-cell boundaries to differing extents, and these isotypes are considerably absent from the nucleus (Pauken & Capco, 1999. During the late eight-cell stage just prior to compaction the isotype is greatly enriched in the nuclei (Pauken & Capco, 2000).…”
Section: The Early Embryomentioning
confidence: 99%
“…Moreover, when PKC was experimentally activated by the natural agonist (DiC8 a diacylglycerol and natural activator of PKC) it induces PKC to localize at internal cell-cell boundaries. Then -catenin becomes phosphorylated and accumulates at these internal cell-cell boundaries as the blastomeres begin to flatten out on each other during the process of embryonic compaction (Pauken & Capco, 1999). In addition, it was shown that immediately before compaction beginscatenin becomes part of the detergent-resistant cytoskeleton at intercellular boundaries indicative of its association with the adherens junctions that are responsible for adhering and subsequently flattening of the blastomeres later during compaction (Pauken & Capco, 1999).…”
“…β-catenin, which is phosphorylated on ser/thr residues at the time of compaction, is likely to be a target of this signaling cascade. (Goval et al, 2000;Pauken and Capco, 1999). The cytoskeleton protein ezrin is another good candidate (Louvet-Vallée et al, 2001).…”
Please cite this article as: Dard, N., Breuer, M., Maro, B., Louvet-Vallée, S., Morphogenesis of the mammalian blastocyst, Molecular and Cellular Endocrinology (2007),
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