scholarly journals DEAD-Box Protein-103 (DP103, Ddx20) Is Essential for Early Embryonic Development and Modulates Ovarian Morphology and Function

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2168-2175 ◽  
Author(s):  
Jean-François Mouillet ◽  
Xiaomei Yan ◽  
Qinglin Ou ◽  
Lingling Jin ◽  
Louis J. Muglia ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Micro Rna ◽  
Early Embryonic Development ◽  
Cell Stage ◽  
Steroidogenic Factor 1 ◽  
Multifunctional Protein ◽  
Barr Virus ◽  
Dead Box ◽  
Epstein Barr ◽  
And Function

The DEAD-box helicase DP103 (Ddx20, Gemin3) is a multifunctional protein that interacts with Epstein-Barr virus nuclear proteins (EBNA2/EBNA3) and is a part of the spliceosomal small nuclear ribonucleoproteins complex. DP103 also aggregates with the micro-RNA machinery complex. We have previously shown that DP103 interacts with the nuclear receptor steroidogenic factor-1 (SF-1, NR5A1), a key regulator of reproductive development, and represses its transcriptional activity. To further explore the physiological function of DP103, we disrupted the corresponding gene in mice. Homozygous Dp103-null mice die early in embryonic development before a four-cell stage. Although heterozygous mice are healthy and fertile, analysis of steroidogenic tissues revealed minor abnormalities in mutant females, including larger ovaries, altered estrous cycle, and reduced basal secretion of ACTH. Our data point to diverse functions of murine DP103, with an obligatory role during early embryonic development and also in modulation of steroidogenesis.

scholarly journals Helper cell-independent cytotoxic clones in man.

1982 ◽  
Vol 156 (6) ◽  
pp. 1854-1859 ◽  
Author(s):  
S L Wee ◽  
L K Chen ◽  
G Strassmann ◽  
F H Bach
Keyword(s):  
T Cell ◽  
Epstein Barr Virus ◽  
Helper Cell ◽  
Cytotoxic T Cell ◽  
Lymphoblastoid Cell Lines ◽  
Barr Virus ◽  
Mediate Cytotoxicity ◽  
Epstein Barr ◽  
And Function

We report here a class of helper cell-independent cytotoxic T cell (HITc) clones in man that can proliferate in response to antigenic stimulation as well as mediate cytotoxicity. HITc appear to be rare among clones derived from primary in vitro allosensitized culture, but constitute the majority of clones derived from cells sensitized to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines. The implications of the derivation and function of HITc clones are discussed.

scholarly journals Upregulation of special AT-rich-binding protein 1 by Epstein–Barr virus latent membrane protein 1 in human nasopharyngeal cells and nasopharyngeal cancer

2013 ◽  
Vol 94 (3) ◽  
pp. 507-513 ◽  
Author(s):  
Kazuhira Endo ◽  
Julia Shackelford ◽  
Mitsuharu Aga ◽  
Tomokazu Yoshizaki ◽  
Joseph S. Pagano
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Binding Protein ◽  
Nasopharyngeal Cancer ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Tissue Samples ◽  
Multifunctional Protein ◽  
Barr Virus ◽  
Epstein Barr

A global regulator of chromatin remodelling and gene expression, special AT-rich-binding protein 1 (SATB1) has been implicated in promotion of growth and metastasis of a number of cancers. Here, we demonstrate that the principal oncogene of Epstein–Barr virus (EBV), latent membrane protein 1 (LMP1) upregulates SATB1 RNA and protein expression in human nasopharyngeal cell lines. Silencing of endogenously expressed SATB1 with specific short hairpin RNA decreases cell proliferation and resistance to apoptosis induced by growth factor withdrawal. Additionally, we provide evidence that LMP1-mediated expression of Survivin, a multifunctional protein involved in promoting cell growth and survival, is mediated at least in part by SATB1 in human nasopharyngeal cells. Finally, we show that SATB1 protein levels are elevated in tissue samples from patients with nasopharyngeal carcinoma (NPC), and are directly correlated with the expression of LMP1. Taken together, our results suggest that SATB1 functions as a pro-metastatic effector of LMP1 signalling in EBV-positive NPC.

Analysis of hpf1 expression and function in early embryonic development of zebrafish

2018 ◽  
Vol 228 (2) ◽  
pp. 141-147 ◽  
Author(s):  
Zhen Zhang ◽  
Hongwei Sun ◽  
Yu Chen ◽  
Tianqi Cao ◽  
Zhou Songyang ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Early Embryonic Development ◽  
And Function

scholarly journals Multiple isomers of inositol pentakisphosphate in Epstein-Barr-virus- transformed (T5-1) B-lymphocytes. Identification of inositol 1,3,4,5,6-pentakisphosphate, d-inositol 1,2,4,5,6-pentakisphosphate and l-inositol 1,2,4,5,6-pentakisphosphate

1991 ◽  
Vol 280 (2) ◽  
pp. 323-329 ◽  
Author(s):  
F M McConnell ◽  
L R Stephens ◽  
S B Shears
Keyword(s):  
Inositol Polyphosphate ◽  
Permeabilized Cells ◽  
Barr Virus ◽  
Epstein Barr ◽  
Polyphosphate Metabolism ◽  
And Function ◽  
Lymphocyte Cell ◽  
Lymphocyte Cell Line

Substantial amounts of three [3H]InsP5 isomers were detected in [3H]inositol-labelled human lymphoblastoid (T5-1) cells. Their structures were determined by h.p.l.c. [Phillippy & Bland (1988) Anal. Biochem. 175, 162-166], and by utilizing a stereospecific D-inositol 1,2,4,5,6-pentakisphosphate 3-kinase from Dictyostelium discoideum [Stephens & Irvine (1990) Nature (London) 346, 580-583]. The structures were: inositol 1,3,4,5,6-pentakisphosphate, D-inositol 1,2,4,5,6-pentakisphosphate and L-inositol 1,2,4,5,6-pentakisphosphate. The relative proportions of these isomers (approx. 73:14:14 respectively) were unaffected by cross-linking anti-IgD receptors. The T5-1 cells also contained InsP6 and three Ins P4s, which were identified as the 1,3,4,5, 1,3,4,6 and 3,4,5,6 isomers. In incubations with permeabilized T5-1 cells, both 1,3,4,6 and 3,4,5,6 isomers of InsP4 were phosphorylated solely to Ins(1,3,4,5,6)P5. Permeabilized cells also dephosphorylated InsP6, even in the presence of a large excess of glucose 6-phosphate to saturate non-specific phosphatases. In the latter experiments the following isomers of InsP5 accumulated: D- and/or L-Ins(1,2,3,4,5)P5, plus D- and/or L-Ins(1,2,4,5,6)P5. This demonstration that multiple isomers of InsP5 may be formed in vivo and in vitro by a transformed lymphocyte cell line adds a new level of complexity to the study of inositol polyphosphate metabolism and function.

The requirement for protein kinase C delta (PRKCD) during preimplantation bovine embryo development

2016 ◽  
Vol 28 (4) ◽  
pp. 482 ◽  
Author(s):  
Qi-En Yang ◽  
Manabu Ozawa ◽  
Kun Zhang ◽  
Sally E. Johnson ◽  
Alan D. Ealy
Keyword(s):  
Gene Expression ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Embryonic Development ◽  
Embryo Development ◽  
Early Embryonic Development ◽  
Bovine Embryo ◽  
Bovine Embryos ◽  
Cell Stage ◽  
Kinase C

Protein kinase C (PKC) delta (PRKCD) is a member of the novel PKC subfamily that regulates gene expression in bovine trophoblast cells. Additional functions for PRKCD in early embryonic development in cattle have not been fully explored. The objectives of this study were to describe the expression profile of PRKCD mRNA in bovine embryos and to examine its biological roles during bovine embryo development. Both PRKCD mRNA and protein are present throughout early embryo development and increases in mRNA abundance are evident at morula and blastocyst stages. Phosphorylation patterns are consistent with detection of enzymatically active PRKCD in bovine embryos. Exposure to a pharmacological inhibitor (rottlerin) during early embryonic development prevented development beyond the eight- to 16-cell stage. Treatment at or after the 16-cell stage reduced blastocyst development rates, total blastomere numbers and inner cell mass-to-trophoblast cell ratio. Exposure to the inhibitor also decreased basal interferon tau (IFNT) transcript abundance and abolished fibroblast growth factor-2 induction of IFNT expression. Furthermore, trophoblast adhesion and proliferation was compromised in hatched blastocysts. These observations provide novel insights into PRKCD mRNA expression profiles in bovine embryos and provide evidence for PRKCD-dependent regulation of embryonic development, gene expression and post-hatching events.

RelA and RelB cross-talk and function in Epstein–Barr virus transformed B cells

Leukemia ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 871-879 ◽  
Author(s):  
A Chanut ◽  
F Duguet ◽  
A Marfak ◽  
A David ◽  
B Petit ◽  
...  
Keyword(s):  
B Cells ◽  
Cross Talk ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Epstein Barr ◽  
And Function

scholarly journals DNA methylation and miRNA-1296 act in concert to mediate spatiotemporal expression of KPNA7 during bovine oocyte and early embryonic development

2019 ◽  
Author(s):  
Lei Wang ◽  
Jacqelyn M. Hand ◽  
Liyuan Fu ◽  
George W. Smith ◽  
Jianbo Yao
Keyword(s):  
Dna Methylation ◽  
Embryonic Development ◽  
Early Stage ◽  
Early Embryonic Development ◽  
Hek293 Cells ◽  
Proximal Promoter ◽  
Pcr Analysis ◽  
Coding Region ◽  
Cell Stage ◽  
Cpg Sites

Abstract Background Epigenetic regulation of oocyte-specific maternal factors is essential for oocyte and early embryonic development. KPNA7 is an oocyte-specific maternal factor, which controls transportation of nuclear proteins important for early embryonic development. To elucidate the epigenetic mechanisms involved in the controlled expression of KPNA7, both DNA methylation associated transcriptional silencing and miRNA-mediated mRNA degradation of KPNA7 were examined. Results Comparison of DNA methylation profiles at the proximal promoter of KPNA7 gene between oocyte and 6 different somatic tissues identified 3 oocyte-specific differentially methylated CpG sites. Expression of KPNA7 mRNA was reintroduced in bovine kidney-derived CCL2 cells after treatment with the methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza). Analysis of the promoter region of KPNA7 gene in CCL2 cells treated with 5-Aza showed a lighter methylation rate in all the CpG sites. Bioinformatic analysis predicted 4 miRNA-1296 binding sites in the coding region of KPNA7 mRNA. Ectopic co-expression of miRNA-1296 and KPNA7 in HEK293 cells led to reduced expression of KPNA7 protein. Quantitative real time PCR analysis revealed that miRNA-1296 is expressed in oocytes and early stage embryos, and the expression reaches a peak level in 8-cell stage embryos, coincident with the time of embryonic genome activation and the start of declining of KPNA7 expression. Conclusions These results suggest that DNA methylation may account for oocyte-specific expression of KPNA7, and miRNA-1296 targeting the coding region of KPNA7 is a potential mechanism for KPNA7 transcript degradation during the maternal-to-zygotic transition.

scholarly journals Maternal UHRF1 Is Essential for Transcription Landscapes and Repression of Repetitive Elements During the Maternal-to-Zygotic Transition

2021 ◽  
Vol 8 ◽  
Author(s):  
Yanqing Wu ◽  
Juan Dong ◽  
Shenglei Feng ◽  
Qiang Zhao ◽  
Peng Duan ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Critical Role ◽  
Conditional Knockout ◽  
Developmental Competence ◽  
Early Embryonic Development ◽  
Transcriptional Level ◽  
Cell Stage ◽  
Early Embryos ◽  
Maternal To Zygotic Transition ◽  
Zygotic Genome

Maternal factors that modulate maternal-to-zygotic transition (MZT) are essential for the growth from specialized oocytes to totipotent embryos. Despite several studies, the mechanisms regulating epigenetic reprogramming during MZT remain largely elusive. UHRF1 plays a role in maintaining GC methylation in oocytes and early embryos. However, little is known about its role in mouse MZT. Here, we explored the function of maternal UHRF1 in zygotic genome regulation during early embryonic development in mice. We showed that the conditional knockout (cKO) of UHRF1 in either primordial or growing oocytes causes infertility but differentially affects early embryonic development. UHRF1 deficiency in primordial oocytes led to early embryonic developmental arrest at the two-cell stage, accompanied by significant alterations in global DNA and H3K4me3 methylation patterns. In comparison, UHRF1 ablation in growing oocytes significantly reduced developmental competence from two-cell embryos to blastocysts. At the transcriptional level, the absence of maternal UHRF1 led to aberrant transcriptional regulation of the zygotic genome during MZT at the two-cell stage. Furthermore, we observed that retrotransposable elements in UHRF1-deficient oocytes and embryos were not silenced properly; in particular, the LINE-1 and long terminal repeat (LTR) subfamily were activated abnormally. Collectively, the findings of our study reveal that maternal UHRF1 plays a critical role in establishing the correct epigenetic chromatin reprogramming of early embryos, regulating essential genes during MZT, and preserving genome integrity that drives early embryonic development in mice.

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