A maternal factor affecting mouse blastocyst formation

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 797-802 ◽  
Author(s):  
J.P. Renard ◽  
P. Baldacci ◽  
V. Richoux-Duranthon ◽  
S. Pournin ◽  
C. Babinet
Keyword(s):  
Direct Evidence ◽  
Normal Development ◽  
Functional Inequality ◽  
Preimplantation Embryos ◽  
Mouse Blastocyst ◽  
Maternal Control ◽  
Paternal Genome ◽  
Functional Differences ◽  
Embryonic Genome ◽  
Parental Contribution

Normal development of the mouse embryo requires the presence of both paternal and maternal genomes. This is due to functional differences having their origin in a differential imprinting of parental genomes. Furthermore, several lines of evidence show that the very early interactions between egg cytoplasm and pronuclei may influence the programming of the embryonic genome and modulate the functional inequality of the parental contribution even during preimplantation stages. In this paper, we show that a factor present in ovulated oocytes of the mouse mutant strain DDK and therefore of maternal origin prevents the formation of the blastocyst. This factor, which acts via an interaction with the paternal genome, is present in oocytes as an RNA and is still active in preimplantation embryos. This is the first direct evidence of such a maternal control in the mouse.

Apoptosis in Degenerative Diseases of the Basal Ganglia

1998 ◽  
Vol 4 (4) ◽  
pp. 301-311 ◽  
Author(s):  
Robert E. Burke
Keyword(s):  
Cell Death ◽  
Basal Ganglia ◽  
Programmed Cell Death ◽  
Direct Evidence ◽  
Normal Development ◽  
Dopamine Neurons ◽  
Degenerative Diseases ◽  
Morphological Markers ◽  
Degenerative Disorders ◽  
New Hypothesis

Degenerative disorders of the basal ganglia are characterized by disturbances of motor control. Prototypic examples are Parkinson's disease, which is caused by degeneration of dopamine neurons of the substantia nigra, and Huntington's disease, which is caused by degeneration of neurons of the striatum. In recent years, it has been postulated that some of these disorders may be caused by programmed cell death or apoptosis, a genetically regulated form of cell death. There is clear evidence that apoptosis occurs in neurons of the basal ganglia during normal development, that it can be regulated, and that it can be induced in some animal models of these disorders. Although there is some suggestive direct evidence that apoptosis may occur in the human brain in these disorders, the evidence to date is partial and not yet compelling. Nevertheless, programmed cell death is an important new hypothesis for the pathogenesis of these disorders and warrants vigorous further investigation, particularly with molecular markers in addition to classic morphological markers. The concept of programmed cell death is relevant not only to the pathogenesis of these diseases but also to therapeutic issues, such as transplantation approaches.

scholarly journals Transcript profiling of bovine embryos implicates specific transcription factors in the maternal-to-embryo transition

2019 ◽  
Vol 102 (3) ◽  
pp. 671-679 ◽  
Author(s):  
Yanina S Bogliotti ◽  
Nhi Chung ◽  
Erika E Paulson ◽  
James Chitwood ◽  
Michelle Halstead ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Rna Polymerase Ii ◽  
Gene Activation ◽  
Preimplantation Embryos ◽  
Maternal Mrna ◽  
Embryonic Genome ◽  
Maternal Mrnas ◽  
Low Levels ◽  
Genome Activation ◽  
Further Development

Abstract Full-grown oocytes are transcriptionally quiescent. Following maturation and fertilization, the early stages of embryonic development occur in the absence (or low levels) of transcription that results in a period of development relying on maternally derived products (e.g., mRNAs and proteins). Two critical steps occur during the transition from maternal to embryo control of development: maternal mRNA clearance and embryonic genome activation with an associated dramatic reprogramming of gene expression required for further development. By combining an RNA polymerase II inhibitor with RNA sequencing, we were able not only to distinguish maternally derived from embryonic transcripts in bovine preimplantation embryos but also to establish that embryonic gene activation is required for clearance of maternal mRNAs as well as to identify putative transcription factors that are likely critical for early bovine development.

scholarly journals Histone variant H3.3–mediated chromatin remodeling is essential for paternal genome activation in mouse preimplantation embryos

2018 ◽  
Vol 293 (10) ◽  
pp. 3829-3838 ◽  
Author(s):  
Qingran Kong ◽  
Laura A. Banaszynski ◽  
Fuqiang Geng ◽  
Xiaolei Zhang ◽  
Jiaming Zhang ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Histone Variant ◽  
Preimplantation Embryos ◽  
Paternal Genome ◽  
Genome Activation

scholarly journals Transcription of paternal Y-linked genes in the human zygote as early as the pronucleate stage

Zygote ◽  
1994 ◽  
Vol 2 (4) ◽  
pp. 281-287 ◽  
Author(s):  
Asangla Ao ◽  
Robert P. Erickson ◽  
Robert M.L. Winston ◽  
Alan H Handysude
Keyword(s):  
Mammalian Species ◽  
Blastocyst Stage ◽  
Preimplantation Embryos ◽  
Human Embryos ◽  
Cell Stage ◽  
Gonad Differentiation ◽  
Embryonic Genome ◽  
Human Preimplantation Embryos

SummaryGlobal activation of the embryonic genome occurs at the 4– to 8–cell stage in human embryos and is marked by continuation of early cleavage divisions in the presence of transcriptional inhibitors. Here we demonstrate, using recerse transcripase–polymerase chin reaction (Rt–PCR), the presence of transcripts for wo paternal Y chromosomal genes, ZFY and SRY in human preimplantation embryos. ZFY transcripts were detected as early as the pronucleate stage, 20–24 h post-insemination In vitro and at intermediate stages up to the blastocyst stage. SRY Transcripts were also detected at 2–cell to blastocyos observed in many mammalian species focuses attention on the role of events in six determination prior to gonad differentiation.

Role of peptidylarginine deiminase 4 (PAD4) in pig parthenogenetic preimplantation embryonic development

Zygote ◽  
2012 ◽  
Vol 21 (4) ◽  
pp. 385-393
Author(s):  
Manjula Brahmajosyula ◽  
Masashi Miyake
Keyword(s):  
Gene Regulation ◽  
Embryonic Development ◽  
Normal Development ◽  
Preimplantation Embryos ◽  
Peptidylarginine Deiminase ◽  
Stages Of Development ◽  
Developmental Arrest ◽  
Slow Development ◽  
Arginine Modification

SummaryArginine modification to citrulline (citrullination) is catalyzed by peptidylarginine deiminases (PADs) and one of the isomers PAD4 is shown to be involved in the gene regulation. In our previous paper we studied the localization and expression of PAD4 and the target of PAD4 in mammalian gametes and preimplantation embryos. In this study the role of PAD4 was examined in the pig diploid parthenogenetic preimplantation embryonic development. Knockdown of PAD4 by RNAi resulted in delayed development. Inhibition of PAD4 by a potent PAD4 inhibitor Cl-amidine from the time of activation for 24 h resulted in developmental arrest at the first cleavage. Inhibition at the later stages of development resulted in delayed or arrested development. A shorter exposure to Cl-amidine for 6 h at any stage of growth resulted in slow development. Thus, this study suggests that PAD4 activity is essential for the normal development of the embryos.

scholarly journals Phosphatidylinositol 3-kinase signaling in mammalian preimplantation embryo development

Reproduction ◽  
2008 ◽  
Vol 136 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Chris O'Neill
Keyword(s):  
Embryo Development ◽  
Normal Development ◽  
Preimplantation Embryo ◽  
Preimplantation Embryos ◽  
External Information ◽  
Ph Domain ◽  
Phosphatidylinositol 3 Kinase ◽  
Preimplantation Embryo Development ◽  
Wide Range ◽  
Phosphatidylinositol 3

The development of the preimplantation mammalian embryo is an autopoietic process; once initiated development proceeds without an absolute requirement for external information or growth cues. This developmental autonomy is partly explained by the generation of autocrine trophic ligands that are released and act back on the embryo via specific receptors. Several embryotrophic ligands cause receptor-dependent activation of 1-o-phosphatidylinositol 3-kinase. This enzyme phosphorylates phosphatidylinositol-4,5-bisphosphate to form phosphatidylinositol-3,4,5-trisphosphate. Genetic or pharmacological ablation of this enzyme activity disrupts normal development of preimplantation embryos. Phosphatidylinositol-3,4,5-trisphosphate is a membrane lipid that acts as a docking site for a wide range of proteins possessing the pleckstrin homology (PH) domain. Such proteins are important regulators of cell survival, proliferation, and differentiation. RAC-α serine/threonine protein kinase is an important PH domain protein and its activity is required for normal preimplantation embryo development and survival. The activity of a range of PH domain proteins is also implicated in the normal development of the embryo. This review critically examines the evidence for the activation of 1-o-phosphatidylinositol 3-kinase in the generation of pleiotypic trophic response to embryotrophins in the autopoietic development of the preimplantation embryo.

scholarly journals Quantitative analysis of RNA abondance for CTCF during reprogramming of bovine embryo from oocyte to blastocyst

2015 ◽  
Vol 58 (1) ◽  
pp. 171-175
Author(s):  
M. Amiri Roudbar ◽  
H. Dehghani ◽  
M. Tahmoorespur ◽  
A. Zahmatkesh ◽  
H. Adeldust ◽  
...  
Keyword(s):  
Transcriptional Repression ◽  
Developmental Stages ◽  
Mature Oocyte ◽  
Preimplantation Embryos ◽  
Bovine Embryo ◽  
Immature Oocytes ◽  
Embryonic Genome ◽  
Maternal Effect Gene ◽  
Regulatory Functions ◽  
Genome Activation

Abstract. CTCF is a highly conserved protein among eukaryotes and it is involved in many of regulatory functions including, transcriptional repression and activation, chromatin insulation, imprinting, X chromosome inactivation, higher-order chromatin organization, and alternative splicing. Studies performed on mouse embryos indicate that CTCF can be a maternal-effect gene, and is essential for normal development of embryos. CTCF can be used as a molecular effector for the proper epigenetic establishment of embryonic development. The aim of this study was to determine changes in transcript levels of the CTCF gene in bovine preimplantation embryos. RNA was extracted from immature and mature oocytes and embryos at various developmental stages (two-cell, four-cell, eight-cell, and blastocysts). Results showed that the amounts of CTCF transcripts decreased in mature oocyte in comparison with immature oocytes, but this change was not significant. In addition, the amount of CTCF transcript in embryos at two-cell, four-cell, eight-cell, and blastocyst stages significantly increased in comparison with immature oocytes. These data show that CTCF expression in bovine embryo begins at minor embryonic genome activation.

scholarly journals Mitotic fidelity requires transgenerational action of a testis-restricted HP1

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Mia T Levine ◽  
Helen M Vander Wende ◽  
Harmit S Malik
Keyword(s):  
Chromosome Segregation ◽  
Mitotic Spindle ◽  
Sperm Chromatin ◽  
Transgenerational Effect ◽  
Maternal Control ◽  
Paternal Genome ◽  
Heterochromatin Protein ◽  
Sister Chromatids ◽  
Maternal Genome ◽  
Sperm Dna

Sperm-packaged DNA must undergo extensive reorganization to ensure its timely participation in embryonic mitosis. Whereas maternal control over this remodeling is well described, paternal contributions are virtually unknown. In this study, we show that Drosophila melanogaster males lacking Heterochromatin Protein 1E (HP1E) sire inviable embryos that undergo catastrophic mitosis. In these embryos, the paternal genome fails to condense and resolve into sister chromatids in synchrony with the maternal genome. This delay leads to a failure of paternal chromosomes, particularly the heterochromatin-rich sex chromosomes, to separate on the first mitotic spindle. Remarkably, HP1E is not inherited on mature sperm chromatin. Instead, HP1E primes paternal chromosomes during spermatogenesis to ensure faithful segregation post-fertilization. This transgenerational effect suggests that maternal control is necessary but not sufficient for transforming sperm DNA into a mitotically competent pronucleus. Instead, paternal action during spermiogenesis exerts post-fertilization control to ensure faithful chromosome segregation in the embryo.

131 DYNAMICS OF HISTONE H3 METHYLATION AT POSITIONS K4 AND K9 IN MOUSE, RABBIT, AND BOVINE PRE-IMPLANTATION EMBRYOS

2006 ◽  
Vol 18 (2) ◽  
pp. 174 ◽  
Author(s):  
K. Lepikhov ◽  
F. Yang ◽  
C. Wrenzycki ◽  
V. Zakhartchenko ◽  
H. Niemann ◽  
...  
Keyword(s):  
Histone H3 ◽  
Distribution Patterns ◽  
Blastocyst Stage ◽  
Dna Demethylation ◽  
Preimplantation Embryos ◽  
Staining Procedure ◽  
Cell Stage ◽  
Paternal Genome ◽  
Histone H3 Methylation ◽  
Rabbit Embryos

In mammals, upon the penetration of sperm into the oocyte, the paternal genome undergoes dramatic epigenetic changes. Protamin packaging of DNA is replaced by histones that acquire specific modifications. In mouse zygotes, paternal DNA gets rapidly demethylated by an active mechanism. In bovine zygotes the methylation from paternal DNA is erased only partially, and in rabbit zygotes it persists at the initial level. To understand whether these reprogramming differences are also reflected in histone modifications, we examined the dynamic changes of histone H3 methylation at positions K4 and K9 in mouse, bovine, and rabbit zygotes and in preimplantation embryos using an immunofluorescence staining procedure (Lepikhov and Walter 2004 BMC Dev. Biol. 4, 12). In zygotes, maternal chromatin contains both types of histone H3 methylation. After fertilization protamines in sperm are very quickly replaced by histones. After the formation of nucleosomes, histone H3 acquires methylation at position K4 in a stepwise manner: first as mono-methylated form and later as tri-methylated. In the late zygote, both paternal and maternal pronuclei show equal levels of histone H3 methylation at position K4. Regardless of the differences in DNA reprogramming in these 3 species, H3/K9 di-methylation is not detected on paternal genomes and is only associated with maternal genomes. During the subsequent cleavage stages, H3/K9 di-methylation decreases gradually and becomes hardly detectable in 4-cell bovine and rabbit embryos. In mouse embryos, it is detectable through all the stages. Bovine embryos reacquire this type of modification at the 8-16 cell stage, and it remains at the very low levels in rabbit, embryos until the blastocyst stage. In conclusion, mouse, rabbit and bovine zygotes show similar patterns of H3/K4triMe and H3/K9diMe distribution despite the difference in paternal DNA demethylation. The dynamics of H3/K9diMe distribution patterns in cleavage stage embryos from all embryos do not correlate with embryonic genomic activation events.

scholarly journals PKC signalling regulates tight junction membrane assembly in the pre-implantation mouse embryo

Reproduction ◽  
2004 ◽  
Vol 127 (6) ◽  
pp. 653-667 ◽  
Author(s):  
Judith J Eckert ◽  
Amanda McCallum ◽  
Andrew Mears ◽  
Martin G Rumsby ◽  
Iain T Cameron ◽  
...  
Keyword(s):  
Tight Junction ◽  
Normal Development ◽  
Epithelial Differentiation ◽  
Cell Contact ◽  
Contact Pattern ◽  
Mouse Blastocyst ◽  
Membrane Assembly ◽  
Kinase C ◽  
Protein Membrane ◽  
Pkc Activation

Epithelial differentiation including tight junction (TJ) formation occurs exclusively within the trophectoderm (TE) lineage of the mouse blastocyst. Here we examine mechanisms by which TJ protein membrane assembly might be regulated by protein kinase C (PKC) in the embryo. To overcome the inherent staging asynchrony of individual blastomeres within intact embryos, we have used isolated inner cell masses (ICMs) from early blastocysts to induce epithelial differentiation in their outer cells responding to their new cell contact pattern. Two TJ proteins examined retain their order of membrane assembly in isolated ICMs in culture as during normal development (early-assembling ZO-2 and late-assembling ZO-1α+), but this process is highly accelerated. Using six chemical modulators of PKC activity, we show here that PKC signalling is involved in the regulation of TJ membrane assembly. While indolactam-mediated PKC activation stimulates membrane assembly of both TJ proteins, TPA-mediated PKC activation stimulates only that of ZO-1α+. The PKC inhibitors Ro-31-8220, Ro-31-8425 and Gö 6983 suppress the stimulatory effect of both PKC activators on membrane assembly to varying extents according to inhibitor and TJ protein examined. Gö 6983 similarly inhibits ZO-2 and ZO-1α+ membrane assembly. PKC inhibition by Gö 6976 appeared to stimulate TJ membrane assembly. Despite the broad PKC isotype specificity of the inhibitors used, these data suggest that the two TJ proteins are differently regulated by PKC isotypes or subfamilies. As Gö 6983 uniquely affects aPKC (particularly PKCζ) and we find that both PKCδ and ζ relocate upon activator treatment to colocalise partially with the TJ proteins in isolated ICMs, we suggest that at least PKCδ and ζ may play a central role in regulating TJ membrane assembly.

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