Roadmap to embryo implantation: clues from mouse models

Wang, Haibin; Dey, Sudhansu K.

doi:10.1038/nrg1808

Cited by 1,130 publications

(1,130 citation statements)

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“…Wdr1 KO MEF cells have growth defects such as losing S phase and abnormal actin plaques, similar to the phenotypes observed in Wdr1-specific KO cardiomyocytes and sertoli cells (30,31). For successful development, mouse trophoblast cells dramatically differentiate and proliferate, accompanying tremendous changes in cytoskeleton after implantation (39,40). Although the exact reason that WDR1 loss of function results in the embryonic arrest at E5.5 is unclear, the role of WDR1 in actin cytoskeleton might be critical in the differentiation and growth of trophoblast cells.…”

Section: Discussionmentioning

confidence: 58%

Trp-Asp (WD) Repeat Domain 1 Is Essential for Mouse Peri-implantation Development and Regulates Cofilin Phosphorylation

Xiao

Wan

et al. 2017

Journal of Biological Chemistry

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Edited by Xiao-Fan WangTrp-Asp (WD) repeat domain 1 (WDR1) is a highly conserved actin-binding protein across all eukaryotes and is involved in numerous actin-based processes by accelerating Cofilin severing actin filament. However, the function and the mechanism of WDR1 in mammalian early development are still largely unclear. We now report that WDR1 is essential for mouse periimplantation development and regulates Cofilin phosphorylation in mouse cells. The disruption of maternal WDR1 does not obviously affect ovulation and female fertility. However, depletion of zygotic WDR1 results in embryonic lethality at the periimplantation stage. In WDR1 knock-out cells, we found that WDR1 regulates Cofilin phosphorylation. Interestingly, WDR1 is overdosed to regulate Cofilin phosphorylation in mouse cells. Furthermore, we showed that WDR1 interacts with Lim domain kinase 1 (LIMK1), a well known phosphorylation kinase of Cofilin. Altogether, our results provide new insights into the role and mechanism of WDR1 in physiological conditions.The actin cytoskeleton is a highly dynamic structure that regulates cell motility, adhesion, division, and growth and has a fundamental function in embryonic development (1-3). In physiological conditions, actin filaments are continually assembled and disassembled in response to varied cellular activities (4, 5). The dynamics of F-actin is well orchestrated by a large number of actin-binding proteins (5, 6). Actin-depolymerizing factor Cofilin plays critical roles in the modulation of actin cytoskeleton dynamics (7). In vitro, Cofilin severs actin filament at low concentrations, whereas it fully decorates actin filaments and suppresses the severing activity at high concentrations (8, 9). In addition, Cofilin severing F-actin is not explained well for how the filaments of actin cytoskeleton can be rapidly disassembled in physiological conditions (4). Thus, the function of Cofilin in actin dynamics depends not only on its relative concentration to actin, but also on other regulatory proteins in vivo. Dysfunction of these regulating proteins results in aberrant actin cytoskeleton in various cellular and developmental processes (10 -12).Cofilin directly binds with actin to function as a regulator of the actin dynamics (13). However, the phosphorylation of Cofilin at Ser-3 blocks its binding site to actin (14, 15). Thus, the activity of Cofilin is controlled by phosphorylation and dephosphorylation processes, which are regulated by cascade reactions of several protein kinases and phosphatases. Lim domain kinases (LIMKs) 4 and testis-specific protein kinases (TESKs) are responsible for the phosphorylation of Cofilin, whereas slingshot (SSH) family protein phosphatases and pyridoxal phosphatase (PDXP) catalyze the dephosphorylation reaction (16 -20). These kinases and phosphatases are also regulated by their phosphorylation or localization in cytoplasm to maintain the level of Cofilin phosphorylation in response to extracellular stimuli (21-23).The activity of Cofilin on actin disassembly is gr...

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Section: Discussionmentioning

confidence: 58%

Trp-Asp (WD) Repeat Domain 1 Is Essential for Mouse Peri-implantation Development and Regulates Cofilin Phosphorylation

Xiao

Wan

et al. 2017

Journal of Biological Chemistry

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“…1), it is not likely that the disruption of methionine metabolism caused the developmental arrest through inhibition of ZGA. However, ZGA is followed by further transcriptional activation of embryonic genes including those related to morula to blastocyst development [41,42]. Thus, it is possible that the disruption of methionine metabolism affected the gene activation following ZGA.…”

Section: Discussionmentioning

confidence: 99%

Importance of Methionine Metabolism in Morula-to-blastocyst Transition in Bovine Preimplantation Embryos

Ikeda

Sugimoto

Kume

2012

Journal of Reproduction and Development

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Abstract. The roles of methionine metabolism in bovine preimplantation embryo development were investigated by using ethionine, an antimetabolite of methionine. In vitro produced bovine embryos that had developed to the 5-cell stage or more at 72 h after the commencement of in vitro fertilization (IVF) were then cultured until day 8 (IVF = day 0) in medium supplemented with 0 (control), 1, 5 and 10 mM ethionine. Compared with the blastocyst development in the control (40.0%), ethionine at 10 mM almost completely blocked blastocyst development (1.1%, P<0.001), and this concentration was used in the following experiments. Methionine added at the same concentration (10 mM, a concentration control of ethionine) did not cause such an intense developmental inhibition. Development to the compacted morula stage on day 6 was not affected by 10 mM ethionine treatment. S-adenosylmethionine (SAM) added to the ethionine treatment partly restored the blastocyst development. Semiquantitative reverse transcription-polymerase chain reaction analysis of cell lineage-related transcription factors in day 6 compacted morulae showed that the expressions of NANOG and TEAD4 were increased by ethionine treatment relative to the control (P<0.01). Furthermore, immunofluorescence analysis of 5-methylcytosine revealed that DNA was hypomethylated in the ethionine-treated day 6 morulae compared with the control (P<0.001). These results demonstrate that the disruption of methionine metabolism causes impairment of the morula-toblastocyst transition during bovine preimplantation development in part via SAM deficiency, indicating the indispensable roles of methionine during this period. The disruption of methionine metabolism may cause hypomethylation of DNA and consequently lead to the altered expression of developmentally important genes, which then results in the impairment of blastocyst development. Key words: Bovine, Methionine, One-carbon metabolism, Preimplantation embryo, S-adenosylmethionine (J. Reprod. Dev. 58: [91][92][93][94][95][96][97] 2012) M ethionine is a dietary essential amino acid that plays multiple biological roles, including those as the initiating amino acid in eukaryotic protein synthesis, a precursor of the essential methyl donor for methylation reactions (S-adenosylmethionine, SAM) and a source of redox regulators (cysteine and glutathione) [1,2]. Methionine metabolism can be seen as the trans-and remethylation cycle of methionine (methionine cycle) that intertwines with the cycle of folate metabolism (folate cycle) and the transsulfuration pathway from homocysteine, an intermediate in the methionine cycle [3], and these combined metabolic networks are called one-carbon metabolism [4,5]. Recently, mammalian oocytes and preimplantation embryos have been reported to express the key regulatory enzymes in one-carbon metabolism [6][7][8], suggesting that mammalian oocytes and preimplantation embryos can independently utilize and metabolize nutrients in one-carbon metabolism, such as methionine, choline, betaine, folates a...

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“…In mice, the gestation length is about 20 d when counted from the day of vaginal plug formation (day 1). The main biological events occurred within the uteri are embryo implantation, decidualization, placentation and labor [19][20][21], which mainly under the influence of ovarian progesterone and estrogen [22]. A preovulatory estrogen surge induces remarkable proliferation of uterine epithelial cells on day 1 [23,24], while rising levels of progesterone together with preimplantation estrogen secreted on the morning of day 4 induce stromal cell proliferation to establish an optimal milieu for blastocyst attach-ment to the uterine lining [25].…”

Section: Uterine Physiological Role In Normal Reproductive Eventsmentioning

confidence: 99%

Determinants of uterine aging: lessons from rodent models

Kong

Zhang

Chen

et al. 2012

Sci. China Life Sci.

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The uterus is an indispensable organ for the development of a new life in eutherian mammals. The female mammalian reproductive capacity diminishes with age. In this respect, the senescence of uterine endometrium is convinced to contribute to this failure. This review focuses on the physiological function of the uterus and the related influence of aging mainly in rodent models. A better understanding of the underlying mechanisms governing the process of uterine aging is hoped to generate new strategies to prolong the reproductive lifespan in humans. . More importantly, this phenomenon of continuous decline of fecundity with age has also been confirmed in women over 35 years old [10][11][12]. The success of reproduction in eutherian mammals requires the uterus, a unique organ in the viviparity compared to other organisms ensuring full development of the new life in the maternal body [13]. The endometrial environment of uteri is proved to be one of the critical aspects to determine the reproductive capacity [14] and uterine factor has been proved to be critical for the decline of fecundity in both rodents and humans [4,15]. Most of the available information on uterine aging derives from studies on rats and mice [16]. In these species, life span is short and aging animal model can be easily established. This review focuses on the physiological function of the uterus and the related influence of aging mainly in rodent models. determinants, uterine aging, rodent models

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Roadmap to embryo implantation: clues from mouse models

Cited by 1,130 publications

References 127 publications

Trp-Asp (WD) Repeat Domain 1 Is Essential for Mouse Peri-implantation Development and Regulates Cofilin Phosphorylation

Trp-Asp (WD) Repeat Domain 1 Is Essential for Mouse Peri-implantation Development and Regulates Cofilin Phosphorylation

Importance of Methionine Metabolism in Morula-to-blastocyst Transition in Bovine Preimplantation Embryos

Determinants of uterine aging: lessons from rodent models

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