Nuclear structure in early mouse embryos: A comparative ultrastructural and immunocytochemical study with special emphasis on the “2-cell block in vitro”

Bogolyubova, I. O.; Bogoliubova, N.A.; Bogolyubov, D. S.; Parfenov, V. N.

doi:10.1016/j.tice.2006.09.002

Cited by 8 publications

(5 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, 2-cell embryos that fail to cleave but are not dying contain 1–2 large NPBs compared to 11–13 smaller NPBs in embryos that proceed into the second cleavage. 34 These collective observations suggest that the morphology of nuclei in preimplantation embryos may be linked to the transcriptional status of the embryo, therefore further exploration on CDC14B’s role during nucleologenesis will shed light on how the NPBs and cell cycle regulators are connected to zygotic genome activation.…”

Section: Discussionmentioning

confidence: 99%

Over-expression of CDC14B causes mitotic arrest and inhibits zygotic genome activation in mouse preimplantation embryos

Buffone¹,

Schindler²,

Schultz³

2009

Cell Cycle

View full text Add to dashboard Cite

Following fertilization the transition from a highly differentiated oocyte to a totipotent 2-cell embryo requires two unique mitotic cell cycles. The first cell cycle is characterized by a prolonged G1 phase, DNA replication (S phase) that occurs separately in the female and male pronuclei, and a short G2 phase that occur in the absence of cell growth. During the second cell cycle, G1 is short whereas G2 is prolonged and occurs concurrently with zygotic genome activation, which is essential for progression past the 2-cell stage. CDC14B, a dual specificity phosphatase that counteracts cyclin dependent kinase 1 (CDK1/CDC2A) action, regulates mitosis in somatic cells and prevents premature meiotic resumption in mouse oocytes. It is not known if CDC14B plays a role during the unique mitotic cell cycles of preimplantation development. We report that CDC14B is present in mouse embryos and localizes to mitotic centrosomes and spindles. overexpressing CDC14B in 1-cell embryos results in 40% and 60% of the embryos arresting at the 1- and 2-cell stages, respectively. embryos arrested at the 1-cell stage contained reduced CDC2A activity, whereas embryos arrested at the 2-cell stage were in G2 and failed to activate the zygotic genome. In contrast, overexpressing CDC14B in meiotically-incompetent oocytes, which are arrested in a G2-like state and are transcriptionally active, does not repress global transcription. these data suggest that CDC14B is a negative regulator of the 1-to-2-cell transition and of zygotic genome activation in mouse embryogenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

Over-expression of CDC14B causes mitotic arrest and inhibits zygotic genome activation in mouse preimplantation embryos

Buffone¹,

Schindler²,

Schultz³

2009

Cell Cycle

View full text Add to dashboard Cite

show abstract

“…In normally-developing 2-cell embryos, the presence of apoptotic features has not yet been documented (Fabian et al ., 2007b). Even 2-cell blocked embryos show no obvious signs of degradation which might characterize aged or dying cells within 3 days after they entered the block (Goddard & Pratt, 1983; Bogolyubova et al ., 2006).…”

Section: Introductionmentioning

confidence: 99%

Apoptotic processes and DNA cytosine methylation in mouse embryos arrested at the 2-cell stage

Fabian

Bukovská

Juhás

et al. 2009

Zygote

View full text Add to dashboard Cite

The present study evaluates the role of apoptotic cell death and DNA methylation reprogramming in early developmental failures occurring in embryos at the 2-cell stage. Mouse 2-cell embryos were cultured in vitro and treated with chemicals that cause developmental arrest and apoptosis (alpha-amanitin, actinomycin D, TNF-alpha). After 24 h, 48 h and 72 h culture, embryos were analysed using cell-death assays (annexin V staining, TUNEL labelling and immunodetection of active caspase-3) and genome methylation assay (immunodetection of 5-methylcytosine). The ability of embryos at the 2-cell stage to undergo apoptotic processes was very low. In arrested embryos, the presence of all evaluated features of apoptosis was recorded only after 72 h culture and their incidence was sporadical. Interestingly, the most frequently observed apoptotic sign was nuclear condensation and the timing of its appearance preceded even the phosphatidylserine flip. Both normally developing and arrested embryos displayed reduction in DNA cytosine methylation. In arrested embryos, this process was independent of cellular cleavage, was more pronounced and finished in almost complete demethylation of the embryonic genome. The timing of the demethylation overlapped with the onset of major apoptotic events. Although observed apoptotic cells showed either demethylated or methylated DNA cytosine in their nuclei, at blastocyst stage the demethylated status appeared more frequently in them.

show abstract

“…Bogolyubova et al and Qui et al argue, however, that the "in vitro two-cell block" is more than just an artifact of in vitro embryonic development [10,52]. Blocked embryos showed a delay in zygotic gene activation [52].…”

Section: Discussionmentioning

confidence: 99%

“…The nuclear distribution of RNA polymerase II and splicing factors in the two-cell blocked embryos, however, significantly differed from that in normal embryos. These results indicate that the two-cell block reflects fundamental mechanisms of early mammalian development [10]. In this study, we used minimal media to easily identify key factors in the phenomenonological aspects of the two-cell block.…”

Section: Discussionmentioning

confidence: 99%

Acetylcholine rescues two-cell block through activation of IP3 receptors and Ca2+/calmodulin-dependent kinase II in an ICR mouse strain

Cho¹,

Yoon

Hur

et al. 2009

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

Acetylcholine (ACh) causes early activation events in mouse oocytes, but little is known about its precise role in the early embryonic development of mice. We aimed to determine whether and how ACh is capable of rescuing two-cell block in an in vitro culture system. ACh evoked different transient Ca(2+) patterns showing a higher Ca(2+) peak in the two-cell stage embryos (two-cells) than observed in mature oocytes. In early two-cells subjected to an in vitro two-cell block, xestospongin C (Xes-C), an IP3 receptor antagonist, significantly decreased the level of the ACh-induced Ca(2+) increase. The reduction in the ACh-induced Ca(2+) increase by Xes-C in late two-cells was lower than that in early two-cells. Furthermore, KN62 and KN93, both CaMKII inhibitors, were found to reduce the magnitude of the ACh-induced Ca(2+) increase in early two-cells. The addition of ACh to the culture medium showed an ability to rescue in vitro two-cell block. However, the addition of ACh together with both Xes-C and CaMKII inhibitors or with either inhibitor separately had no effect on the rescue of two-cell block. Long-term exposure of late two-cells to ACh decreased morula and early blastocyst development and ACh had a differential effect on early and late two-cells. These results indicate that ACh likely rescues the in vitro two-cell block through activation of IP3R- and/or CaMKII-dependent signal transduction pathways.

show abstract

Nuclear structure in early mouse embryos: A comparative ultrastructural and immunocytochemical study with special emphasis on the “2-cell block in vitro”

Cited by 8 publications

References 35 publications

Over-expression of CDC14B causes mitotic arrest and inhibits zygotic genome activation in mouse preimplantation embryos

Over-expression of CDC14B causes mitotic arrest and inhibits zygotic genome activation in mouse preimplantation embryos

Apoptotic processes and DNA cytosine methylation in mouse embryos arrested at the 2-cell stage

Acetylcholine rescues two-cell block through activation of IP3 receptors and Ca2+/calmodulin-dependent kinase II in an ICR mouse strain

Contact Info

Product

Resources

About