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PurposeThe purpose is to examine the cross-level relationship between workplace fun and informal learning with workplace friendship as a mediator and team climate as a moderator.Design/methodology/approachAdopting a two-wave survey procedure, data were collected from 251 employees working across 45 teams of a leading heat transfer manufacturer in Asia. Hierarchical linear modeling was used to test our hypothesized cross-level moderated mediation model.FindingsOut of the three forms of workplace fun, only two – manager support for fun and coworker socializing – supported our hypotheses. Therefore, not all types of workplace fun are equal and one of the key factors through which fun influences informal learning is by maintaining harmonious interpersonal interactions and high relationship quality in teams.Originality/valueBased on social interdependence theory, this study uncovers the cross-level mechanism of how workplace fun affects informal learning. The findings extend existing research on workplace fun by focusing on not only individual factors but also interpersonal and contextual elements. The findings also provide practical implications for managers to understand the possible impact of workplace fun on employees' informal learning.

This study examines the relationship between corporate social responsibility (CSR) and the auditor’s commitment to internal control which strengthens the internal control system and reduces fraud. ...

Purpose As the capital market in China is still developing, several constraints on a Chinese-listed firm’s financing strategy have a direct impact on its financial flexibility. The purpose of this paper is to reconstruct traditional financial flexibility index (FFI) derived from the western context, provide empirical evidence within eastern context by modified FFI and examine how the managerial efficiency of Chinese-listed firms is demonstrated with modified FFI to escort corporate life cycle hypothesis. Design/methodology/approach By tailored FFI to fit the contemporary operations of Chinese-listed firms, this study investigates how managerial efficiency varies across different life stages to demonstrate the moderating power in the firm performance of financially flexible firm. Findings It is found that financially flexible firms in the Chinese stock market generally experience good firm performance, yet the managerial efficiency could gradually be diminishing at their mature stage even firms’ financial flexibility remains consistent with the agency theory. This paper sheds light on the necessity to reexamine the components in financial flexibility based on the eastern context, and provides avenue to further understand the managerial behavior of Chinese listed firms when considering firm life cycles. Research limitations/implications Although it is difficult for this current study to offer the precise weights on each factor in calculating financial flexibility, the judgment matrix method is adopted to at least provide reliable estimates in accordance with Chinese business contexts with less than 10 percent errors in contrast to the actual weights. Practical implications This modified FFI is particularly suitable for Chinese-listed firms under certain unique financial reporting regulations by adjusting a number of weights and factors. This study may help practitioners understand the managerial conduct of publicly listed firms in China. Originality/value The paper constructs a modified FFI with Chinese stock market characteristics embedded, and provides insightful evidence to explain the new pecking order theory by considering the life cycle stage of Chinese-listed companies.

Endometriosis is the major cause of female infertility and has been linked to the action of estrogen and estrogen receptor (ER). A new pool of ERβ locates within mitochondria, which regulates the endometriotic cell withstanding external insults, but its effect remains controversial. We hypothesize that mitochondrial estrogen receptor ERβ (mtERβ) is a pivotal regulator in estradiol-mediated cell protection leading to the endometriotic progression. We observed elevated levels of ERβ in the endometriotic tissues. A dramatic increase of ERβ in mitochondria (mtERβ) was found in the ectopic endometriotic tissues, or the estradiol-primed primary endometriotic cells. We analyzed the mtERβ-specific overexpressing clone (mtsERβ), which exhibited higher mitochondrial bioenergetics and lower reactive oxygen species (ROS) generation. The mtsERβ-overexpressed endometriotic cells displayed an enhanced migration phenotype, whereas significantly attenuated migration by mitochondrial respiratory inhibitor (oligomycin) or ERβ deficiency by shERβ. Further investigations revealed that ERβ directly modulated mitochondrial DNA (mtDNA) gene expression by interacting with mtDNA D-loop and polymerase γ. The mtsERβ afforded a resistance to oxidative insult-induced apoptosis through the induction of the ROS scavenger enzyme Mn-superoxide dismutase and anti-apoptotic protein Bcl-2. Collectively, the demonstration of mtERβ responses in restoration of mitochondrial bioenergetics and inhibition of mitochondria-dependent apoptotic events provides insight into the pathogenesis of endometriosis, suggesting ERβ-selective estrogen receptor modulator may serve as novel therapeutics of endometriosis in the future.

Si-Wu Tang (SWT), a traditional Chinese formula, is commonly used for treating female diseases, such as relief of menstrual discomfort and climacteric syndrome. The aim of this study was to explore the synergistic effects between each herb in SWT on menstrual disorder patterns. Estradiol regulation and antioxidative effects were indicators that ameliorated menstrual disorder patterns and the total polyphenol and polysaccharide contents were quality markers. According to relationships of bioactivity and phytochemical contents, we discuss the effects of each herb in SWT. In a testosterone-treated MCF-7 cell model, Rehmannia glutinosa and catalpol significantly increased the estradiol content and aromatase upregulation in cell culture. We suggest that catalpol is an aromatase promoter in SWT, and R. glutinosa is a major actor. In terms of the antioxidant activity, pentagalloylglucose, gallic acid, and ferulic acid had stronger antioxidative effects than other compounds. We suggest that the antioxidative ability depends on polyphenols, and Paeonia lactiflora is a major contributor. Based on the prescribing principle of traditional Chinese medicine (TCM) theory, we suggest that R. glutinosa in SWT act as an aromatase promoter in the role of sovereign for ameliorating menstrual disorder patterns. As P. lactiflora has the strongest antioxidant effects and can prevent ROS damage ovarian; therefore, P. lactiflora could help R. glutinosa work as a minister for menstrual disorder patterns and R. glutinosa and P. lactiflora are a herbal pair in SWT.

High mobility group box 1 (HMGB1) is upregulated in nearly every tumor type. Importantly, clinical evidence also proposed that HMGB1 is particularly increased in metastatic prostate cancer patients. Besides, a growing number of studies highlighted that HMGB1 could be a successful therapeutic target for prostate cancer patients. Glycyrrhizin is a novel pharmacological inhibitor of HMGB1 that may repress prostate cancer metastasis. This research was aimed to investigate the effect of glycyrrhizin on inhibition of HMGB1-induced epithelial-to-mesenchymal transition (EMT), a key step of tumor metastasis, in prostate cancer cells. In this study, HMGB1 knock-downed DU145 prostate cancer cells were used. Silencing the HMGB1 gene expression triggered a change of cell morphology to a more epithelial-like shape, which was accompanied by a reduction of Cdc42/GSK-3β/Snail and induction of E-cadherin levels estimated by immunoblotting. Furthermore, HMGB1 facilitated cell migration and invasion via downstream signaling, whereas HMGB1 targeting by 10 mM ethyl pyruvate effectively inhibited EMT characteristics. Interestingly, cell migration capacity induced by HMGB1 in DU145 cells was abolished in a dose-dependent effect of 25-200 μM glycyrrhizin treatment. In conclusion, glycyrrhizin successfully inhibited HMGB1-induced EMT phenomenon, which suggested that glycyrrhizin may serves as a therapeutic agent for metastatic prostate cancer.

The meiotic functions of Emi2, an inhibitor of the APC/C complex, have been best characterized in oocytes where it mediates metaphase II arrest as a component of the cytostatic factor. We generated knockout mice to determine the in vivo functions of Emi2-in particular, its functions in the testis, where Emi2 is expressed at high levels. Male and female Emi2 knockout mice are viable but sterile, indicating that Emi2 is essential for meiosis but dispensable for embryonic development and mitotic cell divisions. We found that, besides regulating cell-cycle arrest in mouse eggs, Emi2 is essential for meiosis I progression in spermatocytes. In the absence of Emi2, spermatocytes arrest in early diplotene of prophase I. This arrest is associated with decreased Cdk1 activity and was partially rescued by a knockin mouse model of elevated Cdk1 activity. Additionally, we detected expression of Emi2 in spermatids and sperm, suggesting potential post-meiotic functions for Emi2.

// Yu-Chen SH Yang 1, * , Yu-Tang Chin 2, * , Meng-Ti Hsieh 2, 3 , Hsuan-Yu Lai 2 , Chien-Chih Ke 4 , Dana R. Crawford 5 , Oscar K. Lee 6 , Earl Fu 7 , Shaker A. Mousa 8 , Patricia Grasso 9 , Leroy F. Liu 2 , Heng-Yu Chang 10, 11 , Heng-Yuan Tang 8 , Hung-Yun Lin 2, 3 , Paul J. Davis 8, 9 1 Joint Biobank, Office of Human Research, Taipei Medical University, Taipei, Taiwan 2 Taipei Cancer Center, Taipei Medical University, Taipei, Taiwan 3 PhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan 4 Biomedical Imaging Research Center, National Yang-Ming University, Taipei, Taiwan 5 Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA 6 Stem Cell Research Center, National Yang-Ming University, Taipei, Taiwan 7 Department of Periodontology, School of Dentistry, National Defense Medical College, Taipei, Taiwan 8 Pharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Albany, New York, USA 9 Department of Medicine, Albany Medical College, Albany, New York, USA 10 Department of Biochemistry and Molecular Cell Biology, College of Medicine, Taipei Medical University, Taipei, Taiwan 11 Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan * These authors have contributed equally to this work Correspondence to: Heng-Yu Chang, e-mail: hychang@tmu.edu.tw Hung-Yun Lin, e-mail: linhy@tmu.edu.tw Keywords: obesity, leptin, OB3-leptin peptide, cancer cell invasion Received: September 15, 2015 Accepted: March 18, 2016 Published: March 30, 2016 ABSTRACT Obesity results in increased secretion of cytokines from adipose tissue and is a risk factor for various cancers. Leptin is largely produced by adipose tissue and cancer cells. It induces cell proliferation and may serve to induce various cancers. OB3-leptin peptide (OB3) is a new class of functional leptin peptide. However, its mitogenic effect has not been determined. In the present study, because of a close link between leptin and the hypothalamic-pituitary-thyroid axis, OB3 was compared with leptin in different thyroid cancer cells for gene expression, proliferation and invasion. Neither agent stimulated cell proliferation. Leptin stimulated cell invasion, but reduced adhesion in anaplastic thyroid cancer cells. Activated ERK1/2 and STAT3 contributed to leptin-induced invasion. In contrast, OB3 did not affect expression of genes involved in proliferation and invasion. In vivo studies in the mouse showed that leptin, but not OB3, significantly increased circulating levels of thyrotropin (TSH), a growth factor for thyroid cancer. In summary, OB3 is a derivative of leptin that importantly lacks the mitogenic effects of leptin on thyroid cancer cells.

This study aims to examine the association between calling and proactive behavior by proposing a moderated mediation model. Drawing from the job crafting perspective, career commitment and job auto...

Although extensive literature has suggested that investor sentiment may be one of the most important factors in explaining investor trading frequency and trading strategies, how individual investors are significantly influenced by sentiment remains underexplored. The feature of numerous individual investors in the Taiwan stock market provides an avenue to examine the relationship of investor sentiment to trading frequency and positive-feedback trading according to intraday data. Using a vector autoregression model to measure feedback trading in one-minute intervals, we find that trading frequency appears to increase in periods of rising market, suggesting that investor sentiment–driven trading increases market trading frequency without relying on past experiences to conduct trading behavior.

To summarize available evidence from randomized-controlled trials which have evaluated triggering of final oocyte maturation with concomitant GnRH agonists and hCG in patients undergoing IVF, and to analyze whether dual triggering is as efficacious as hCG triggering in terms of oocyte and pregnancy outcomes. A comprehensive literature search was performed to identify randomized-controlled trials comparing IVF outcomes between women receiving combined administration of hCG with GnRH agonists and those receiving hCG alone for triggering of final oocyte maturation. Four studies including 527 patients eligible for inclusion in meta-analysis were identified. No significant difference in the number of mature oocytes or fertilized oocytes retrieved was found between groups. Clinical pregnancy rate with dual triggering was significantly higher as compared with hCG-alone triggering (pooled OR = 0.48, 95% CI 0.31–0.77, P = 0.002), but there was no significant difference in the ongoing pregnancy rate between groups. Results of meta-analysis indicate comparable or significantly improved outcomes with the use of GnRH agonists plus hCG as compared with hCG alone for triggering of final oocyte maturation.

Objective: This study was conducted to explore the association between sexual orientations and polycystic ovary syndrome (PCOS)-related parameters. Materials and methods: A cross-sectional study with participants recruited from the regular outpatient clinic at the Department of Obstetrics and Gynecology at Taipei Medical University Hospital, Taipei, Taiwan between July 2012 and December 2013 was carried out. A total of 97 women met the criterion of having been diagnosed with PCOS. Among these 97 women, 89 were heterosexuals and eight were self-identified as lesbians. At the same time, 78 women without PCOS were enrolled to serve as the control group. Participants were given a standard questionnaire and had blood withdrawn for biochemical analysis of androgen parameters—including total testosterone, androstenedione, sex hormone binding globulin, free androgen index, 17β-estradiol (E2), luteinizing hormone, and follicular-stimulating hormone. The biochemical data were measured to compare the PCOS clinical parameters present in people of different sexual orientations (lesbians and heterosexuals). Results: The women with PCOS, regardless of sexual orientation, had higher percentages and serum levels of hyperandrogenism-related clinical parameters than the women without PCOS [acne (87.5% and 60.7% vs. 23.1%), p

Prior evidence shows voluntary recalls do not lead to better abnormal stock returns when compared with involuntary ones, although they intend to convey positive signals. This puzzling evidence can be attributed to the ignorance of information uncertainty associated with different product recall strategies. Because of the mixed managerial motives inherent in business strategy, voluntary recalls may involve greater information uncertainty than involuntary ones that prevent investors from receiving the intended positive messages. This paper argues that corporate social responsibility (CSR) establishes a firm's presence in stakeholder engagement and plays a crucial role in certifying information conveyed by voluntary product recalls. The findings suggest that firms with better CSR performance receive significantly greater firm value change than those with poor CSR performance upon the announcements of voluntary recalls. Besides, the CSR effect is mainly driven by the firm's engagement in technical CSR activities because of the direct dialogues with stakeholders caring about products. Copyright © 2014 John Wiley & Sons, Ltd and ERP Environment

Vertebrate eggs arrest at second meiotic metaphase. The fertilizing sperm causes meiotic exit through Ca(2+)-mediated activation of the anaphase-promoting complex/cyclosome (APC/C). Although the loss in activity of the M-phase kinase CDK1 is known to be an essential downstream event of this process, the contribution of phosphatases to arrest and meiotic resumption is less apparent, especially in mammals. Therefore, we explored the role of protein phosphatase 2A (PP2A) in mouse eggs using pharmacological inhibition and activation as well as a functionally dominant-negative catalytic PP2A subunit (dn-PP2Ac-L199P) coupled with live cell imaging. We observed that PP2A inhibition using okadaic acid induced events normally observed at fertilization: degradation of the APC/C substrates cyclin B1 and securin resulting from loss of the APC/C inhibitor Emi2. Although sister chromatids separated, chromatin remained condensed, and polar body extrusion was blocked as a result of a rapid spindle disruption, which could be ameliorated by non-degradable cyclin B1, suggesting that spindle integrity was affected by CDK1 loss. Similar cell cycle effects to okadaic acid were also observed using dominant-negative PP2Ac. Preincubation of eggs with the PP2A activator FTY720 could block many of the actions of okadaic acid, including Emi2, cyclin B1, and securin degradation and sister chromatid separation. Therefore, in conclusion, we used okadaic acid, dn-PP2Ac-L199P, and FTY720 on mouse eggs to demonstrate that PP2A is needed to for both continued metaphase arrest and successful exit from meiosis.

Previous studies have established that when maturing mouse oocytes are continuously incubated with the Aurora inhibitor ZM447439, meiotic maturation is blocked. In this study, we observe that by altering the time of addition of the inhibitor, oocyte maturation can actually be accelerated by 1 h as measured by the timing of polar body extrusion. ZM447439 also had the ability to overcome a spindle assembly checkpoint (SAC) arrest caused by nocodazole and so rescue polar body extrusion. Consistent with the ability of the SAC to inhibit cyclin B1 degradation by blocking activation of the anaphase-promoting complex, we could also observe a rescue in cyclin B1 degradation when ZM447439 was added to nocodazole-treated oocytes. The acceleration of the first meiotic division by ZM447439, which has not been achieved previously, and its effects on the SAC are all consistent with the proposed mitotic role of Aurora B in activating the SAC. We hypothesize that Aurora kinase activity controls the SAC in meiosis I, despite differences to the mitotic cell cycle division in spindle architecture brought about by the meiotic mono-orientation of sister kinetochores.

Endometriosis is an estrogen-dependent inflammatory disease that affects up to 10% of women of reproductive age and accounts for up to 50% of female infertility cases. It has been highly associated with poorer outcomes of assisted reproductive technology (ART), including decreased oocyte retrieval, lower implantation, and pregnancy rates. A better understanding of the pathogenesis of endometriosis-associated infertility is crucial for improving infertility treatment outcomes. Current theories regarding how endometriosis reduces fertility include anatomical distortion, ovulatory dysfunction, and niche inflammation-associated peritoneal or implantation defects. This review will survey the latest evidence on the role of inflammatory niche in the peritoneal cavity, ovaries, and uterus of endometriosis patients. Nonhormone treatment strategies that target these inflammation processes are also included. Furthermore, mesenchymal stem cell-based therapies are highlighted for potential endometriosis treatment because of their immunomodulatory effects and tropism toward inflamed lesion foci. Potential applications of stem cell therapy in treatment of endometriosis-associated infertility in particular for safety and efficacy are discussed.

While CEOs play a major role in the facilitation of strategic change, little research has documented how a succession CEO, particularly a family CEO successor, affects the strategic change of a fir...

The first female meiotic division (meiosis I, MI) is uniquely prone to chromosome segregation errors through non-disjunction, resulting in trisomies and early pregnancy loss. Here, we show a fundamental difference in the control of mammalian meiosis that may underlie such susceptibility. It involves a reversal in the well-established timing of activation of the anaphase-promoting complex (APC) by its co-activators cdc20 and cdh1. APC(cdh1) was active first, during prometaphase I, and was needed in order to allow homologue congression, as loss of cdh1 speeded up MI, leading to premature chromosome segregation and a non-disjunction phenotype. APC(cdh1) targeted cdc20 for degradation, but did not target securin or cyclin B1. These were degraded later in MI through APC(cdc20), making cdc20 re-synthesis essential for successful meiotic progression. The switch from APC(cdh1) to APC(cdc20) activity was controlled by increasing CDK1 and cdh1 loss. These findings demonstrate a fundamentally different mechanism of control for the first meiotic division in mammalian oocytes that is not observed in meioses of other species.

Mammalian eggs naturally arrest at metaphase of the second meiotic division, until sperm triggers a series of Ca(2+) spikes that result in activation of the anaphase-promoting complex/cyclosome (APC/C). APC/C activation at metaphase targets destruction-box containing substrates, such as cyclin B1 and securin, for degradation, and as such eggs complete the second meiotic division. Cyclin B1 degradation reduces maturation (M-phase)-promoting factor (MPF) activity and securin degradation allows sister chromatid separation. Here we examined the second meiotic division in mouse eggs following expression of a cyclin B1 construct with an N-terminal 90 amino acid deletion (Delta 90 cyclin B1) that was visualized by coupling to EGFP. This cyclin construct was not an APC/C substrate, and so following fertilization, sperm were incapable of stimulating Delta 90 cyclin B1 degradation. In these eggs, chromatin remained condensed and no pronuclei formed. As a consequence of the lack of pronucleus formation, sperm-triggered Ca(2+) spiking continued indefinitely, consistent with a current model in which the sperm-activating factor is localized to the nucleus. Because Ca(2+) spiking was not inhibited by Delta 90 cyclin B1, the degradation timing of securin, visualized by coupling it to EGFP, was unaffected. However, despite rapid securin degradation, sister chromatids remained attached. This was a direct consequence of MPF activity because separation was induced following application of the MPF inhibitor roscovitine. Similar observations regarding the ability of MPF to prevent sister chromatid separation have recently been made in Xenopus egg extracts and in HeLa cells. The results presented here show this mechanism can also occur in intact mammalian eggs and further that this mechanism appears conserved among vertebrates. We present a model in which metaphase II arrest is maintained primarily by MPF levels only.

In the ovary, the paracrine interactions between the oocyte and surrounded granulosa cells are critical for optimal oocyte quality and embryonic development. Mice lacking the androgen receptor (AR−/−) were noted to have reduced fertility with abnormal ovarian function that might involve the promotion of preantral follicle growth and prevention of follicular atresia. However, the detailed mechanism of how AR in granulosa cells exerts its effects on oocyte quality is poorly understood. Comparing in vitro maturation rate of oocytes, we found oocytes collected from AR−/− mice have a significantly poor maturating rate with 60% reached metaphase II and 30% remained in germinal vesicle breakdown stage, whereas 95% of wild-type AR (AR+/+) oocytes had reached metaphase II. Interestingly, we found these AR−/− female mice also had an increased frequency of morphological alterations in the mitochondria of granulosa cells with reduced ATP generation (0.18 ± 0.02 vs. 0.29 ± 0.02 µM/mg protein, p &lt, 0.05) and aberrant mitochondrial biogenesis. Mechanism dissection found loss of AR led to a significant decrease in the expression of peroxisome proliferator-activated receptor γ (PPARγ) co-activator 1-β (PGC1-β) and its sequential downstream genes, nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM), in controlling mitochondrial biogenesis. These results indicate that AR may contribute to maintain oocyte quality and fertility via controlling the signals of PGC1-β-mediated mitochondrial biogenesis in granulosa cells.

While firm innovativeness has been identified as a critical driver of firm growth and survival, the determinants of firm innovativeness have yet sufficiently explored. This study addresses this res...

Our paper establishes the causal links among the driving factor, flexibility degree and performance of a firm and tests these links based on two samples made of American and Chinese listed companies in manufacturing industry respectively from 2009 to 2012. Our results show the financial flexibilities of American and Chinese firms are mainly driven by strengthening risk management and chasing investment opportunities respectively, the degree of financial flexibility has positively impact on firm performance, and the effect of financial flexibility driven by chasing investment opportunities on performance is more statistically significant than financial flexibility driven by strengthening risk management. Our results suggest that a firm can improve its performance if it retains a high flexibility degree driven by chasing investment opportunities.

Metaphase II-arrested mouse eggs are stimulated to complete meiosis by sperm-induced Ca2+ spiking. The Ca2+ signal causes activation of the E3 ligase anaphase-promoting complex/cyclosome (APC), leading to the destruction of key proteins necessary for meiotic exit. We show, using western blots of mouse eggs, the presence of both APC activators cdc20 and cdh1, which target D-box and D-box/KEN-box substrates, respectively, for proteolysis. We decided to examine the temporal activation of APCcdc20 and APCcdh1 by coupling APC substrates to GFP and examining their destruction in real-time following release from second meiotic division arrest. D-box substrates were degraded quickly after the initiation of sperm-induced Ca2+ spiking, such that their degradation was complete by the time of second polar body extrusion. By contrast, KEN-box-containing substrates were degraded when CDK1 activity was low, during the period between polar body extrusion and pronucleus formation. This observation of apparent APCcdh1 activity in meiosis II based on destruction of exogenous GFP-coupled substrates was then confirmed by observing destruction of endogenous APCcdh1 substrates. These data are consistent with a model of initial APCcdc20 activation on sperm-induced activation, followed by APCcdh1 activation after second polar body extrusion. Interestingly, therefore, we propose that mammalian eggs undergo meiosis II with both APCcdc20 and APCcdh1, whereas eggs of other species so far described have APCcdc20 activity only.

While earnings expectation has been shown to determine a firm's investment decisions, little is known about how such expectation influences its horizon of innovation. This paper examines the effect...

Prior research argues that voluntary product recalls are motivated by managers’ intention to convey positive information about recalling firm’s reputation, brand equity and trust-worthiness, and sh...

Spotlights on the action and response behaviors in strategy have augmented our knowledge of competitive interactions, yet a comprehensive understanding on whether responses and nonresponses create ...

Mouse eggs arrest at metaphase II following ovulation and are only triggered to complete meiosis when fertilized. Sperm break the cell cycle arrest by a long-lasting series of Ca2+ spikes that lead to an activation of the anaphase-promoting complex. The signal transduction pathway is not fully resolved but both protein kinase C (PKC) and calmodulin-dependent protein kinase II (CamKII) activities increase at fertilization and previous pharmacological studies have implicated both in cell cycle resumption. Here we used a combination of pharmacological inhibitors and constitutively-active cRNA constructs of PKCα and CamKII microinjected into mouse eggs, to show that it is CamKII and not PKC that is the sufficient trigger for cell cycle resumption from metaphase II arrest. Constitutively active PKC constructs had no effect on meiotic resumption but caused an immediate and persistent elevation in intracellular Ca2+ when store-operated Ca2+ entry was stimulated. With respect to meiotic resumption, the effects of constitutively-active CamKII on eggs were the same as sperm. Eggs underwent second polar body extrusion and pronucleus formation with normal timings; while both securin and cyclin B1 destruction, visualised by coupling to fluorescent protein tags, were complete by the time of polar body extrusion. Induction of a spindle checkpoint by overexpression of Mad2 or by spindle poisons blocked CamKII-induced meiotic resumption but the Ca2+ chelator BAPTA did not. Furthermore direct measurement of Ca2+ levels showed that CamKII did not induce exit from metaphase II arrest by raising Ca2+. Therefore we conclude that PKCs may play an important role in maintaining Ca2+ spiking at fertilization by promoting store-operated Ca2+ entry, while CamKII transduces cell cycle resumption, and lies downstream of sperm-induced Ca2+ release but upstream of a spindle checkpoint. These data, combined with the knowledge that CamKII activity increase at fertilization, suggest that mouse eggs undergo cell cycle resumption through stimulation of CamKII.