scholarly journals A GPI processing phospholipase A2, PGAP6, modulates Nodal signaling in embryos by shedding CRIPTO

2016 ◽  
Vol 215 (5) ◽  
pp. 705-718 ◽  
Author(s):  
Gun-Hee Lee ◽  
Morihisa Fujita ◽  
Katsuyoshi Takaoka ◽  
Yoshiko Murakami ◽  
Yoshitaka Fujihara ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Embryonic Development ◽  
Phospholipase A2 ◽  
Phospholipase D ◽  
Critical Role ◽  
Early Embryonic Development ◽  
Nodal Signaling ◽  
Common Features ◽  
Highly Sensitive ◽  
Anterior Posterior

Glycosylphosphatidylinositol-anchored proteins (GPI-APs) can be shed from the cell membrane by GPI cleavage. In this study, we report a novel GPI-processing enzyme, termed post-glycosylphosphatidylinositol attachment to proteins 6 (PGAP6), which is a GPI-specific phospholipase A2 mainly localized at the cell surface. CRIPTO, a GPI-AP, which plays critical roles in early embryonic development by acting as a Nodal coreceptor, is a highly sensitive substrate of PGAP6, whereas CRYPTIC, a close homologue of CRIPTO, is not sensitive. CRIPTO processed by PGAP6 was released as a lysophosphatidylinositol-bearing form, which is further cleaved by phospholipase D. CRIPTO shed by PGAP6 was active as a coreceptor in Nodal signaling, whereas cell-associated CRIPTO activity was reduced when PGAP6 was expressed. Homozygous Pgap6 knockout mice showed defects in early embryonic development, particularly in the formation of the anterior–posterior axis, which are common features with Cripto knockout embryos. These results suggest PGAP6 plays a critical role in Nodal signaling modulation through CRIPTO shedding.

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.

Cytological observations on fertilization and early embryonic development in sea cucumber Apostichopus japonicus

2012 ◽  
Vol 36 (2) ◽  
pp. 272 ◽  
Author(s):  
Jie TAN ◽  
Hui-ling SUN ◽  
Fei GAO ◽  
Jing-ping YAN ◽  
Ying-hui DONG ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Sea Cucumber ◽  
Apostichopus Japonicus ◽  
Early Embryonic Development

Studies on the early embryonic development of artificially-bred Siberian sturgeon(Acipenser baeri)

2010 ◽  
Vol 34 (5) ◽  
pp. 777-785 ◽  
Author(s):  
Wei SONG ◽  
Jia-kun SONG ◽  
Chun-xin FAN ◽  
Tao ZHANG ◽  
Bin WANG
Keyword(s):  
Embryonic Development ◽  
Siberian Sturgeon ◽  
Early Embryonic Development ◽  
Acipenser Baeri

scholarly journals Unfolded protein response triggers differential apoptotic mechanisms in ovaries and early embryos exposed to maternal type 1 diabetes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Aslı Okan ◽  
Necdet Demir ◽  
Berna Sozen
Keyword(s):  
Embryonic Development ◽  
Er Stress ◽  
Unfolded Protein Response ◽  
Molecular Mechanisms ◽  
Early Embryonic Development ◽  
Unfolded Protein ◽  
Caspase 12 ◽  
Early Embryos ◽  
Protein Response

AbstractDiabetes mellitus (DM) has profound effects on the female mammalian reproductive system, and early embryonic development, reducing female reproductive outcomes and inducing developmental programming in utero. However, the underlying cellular and molecular mechanisms remain poorly defined. Accumulating evidence implicates endoplasmic reticulum (ER)-stress with maternal DM associated pathophysiology. Yet the direct pathologies and causal events leading to ovarian dysfunction and altered early embryonic development have not been determined. Here, using an in vivo mouse model of Type 1 DM and in vitro hyperglycaemia-exposure, we demonstrate the activation of ER-stress within adult ovarian tissue and pre-implantation embryos. In diabetic ovaries, we show that the unfolded protein response (UPR) triggers an apoptotic cascade by the co-activation of Caspase 12 and Cleaved Caspase 3 transducers. Whereas DM-exposed early embryos display differential ER-associated responses; by activating Chop in within embryonic precursors and Caspase 12 within placental precursors. Our results offer new insights for understanding the pathological effects of DM on mammalian ovarian function and early embryo development, providing new evidence of its mechanistic link with ER-stress in mice.

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