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Pop art originated in Britain in 1950, became popular in the United States in the 1960s, and then spread to Italy, Japan and other countries. It pulled art from the high altar, obliterated the boundary between art and life, and made art less inscrutable and obscure, but more affinity. This paper focuses on the pop art style in modern and contemporary art and design works, and discusses the audience's demand for pop art pop culture in the context of contemporary multiculturalism. As a common, popular and commercial art form, pop art has exerted a subtle influence in many fields of design. It emphasizes interest and rebellious spirit, affecting the diversified development of design. This paper is an accurate control of the current design trend, and also a practical exploration of digital redesign of pop art style.

Levels of cotinine, a major metabolite of nicotine, have been positively correlated with risks of cigarette smoking-related diseases. Melatonin is synthesized by the pineal gland and has been demonstrated to be beneficial to oocyte maturation due to its antioxidative activity. In this study, we investigated the effects of cotinine on mouse oocyte meiosis and the protective roles of melatonin in vitro and in vivo. The results showed that cotinine exposure caused defects in the first polar body extrusion and reduced parthenogenetic activation in in vitro-matured oocytes. Additionally, cotinine exposure increased the level of oxidative stress, which resulted in aberrant actin distribution, abnormal spindle morphology, chromosome misalignment, and even oocyte aneuploidy. Simultaneously, cotinine exposure decreased the mitochondrial membrane potential and antioxidant gene expression and increased apoptosis-related gene expression. However, all these toxic effects of cotinine could be reversed after the addition of melatonin, and the mechanism may be a decrease in reactive oxygen species production. In conclusion, cotinine causes poor oocyte quality, which could be rescued by melatonin supplementation during meiotic maturation in mouse oocytes.

Soon after fertilization, the block mechanisms are developed in the zona pellucida (ZP) and plasma membrane of the egg to prevent any additional sperm from binding, penetration, and fusion. However, the molecular basis and underlying mechanism for the post-fertilization block to sperm penetration through ZP has not yet been determined. Here, we find that transglutaminase 2 (Tgm2), an enzyme that catalyzes proteins by the formation of an isopeptide bond within or between polypeptide chains, crosslinks zona pellucida glycoprotein 3 (ZP3) to result in the ZP hardening after fertilization and thus prevents polyspermy. Tgm2 abundantly accumulates in the subcortical region of the oocytes and vanishes upon fertilization. Both inhibition of Tgm2 activity in oocytes by the specific inhibitor in vitro and genetic ablation of Tgm2 in vivo cause the presence of additional sperm in the perivitelline space of fertilized eggs, consequently leading to the polyploid embryos. Biochemically, recombinant Tgm2 binds to and crosslinks ZP3 proteins in vitro, and incubation of oocytes with recombinant Tgm2 protein inhibits the polyspermy. Altogether, our data identify Tgm2 as a participant of zona block to the post-fertilization sperm penetration via hardening ZP surrounding fertilized eggs, extending our current understanding about the molecular basis of block to polyspermy.

Cell adhesion molecule 4 (Cadm4) plays important roles on plasma membrane (PM) to regulate myelin formation and the downregulation of Cadm4 is a prominent feature in many demyelination diseases. However, how Cadm4 maintains its level on PM has been elusive. Here, we identify that Cadm4 is palmitoylated at cysteine-347 (C347) and palmitoylation regulates the stable localization of Cadm4 on PM, as blocking palmitoylation by mutating C347 into alanine (C347A) results in the dissociation of Cadm4 from PM and targeting for degradation. Intriguingly, blocking Cadm4 palmitoylation by introducing C347A (Cadm4-KI) causes myelin abnormalities in CNS, characterized by loss of myelination, myelin infoldings and hypermyelination. Moreover, it is uncovered that Cadm4 palmitoylation is catalyzed by DHHC3, reducing Cadm4 palmitoylation by the deletion of DHHC3 renders the redistribution of Cadm4 for degrading. Consistently, the genetic deletion of DHHC3 leads to downregulated Cadm4 palmitoylation and defects in CNS myelination, virtually phenocopies that of the Cadm4-KI mice. Our findings suggest a mechanism that the stable localization of Cadm4 on PM regulated by protein palmitoylation is vital for myelination in CNS.

Background CK2 (casein kinase 2) is a serine/threonine-selective protein kinase that has been involved in a variety of cellular processes such as DNA repair, cell cycle control and circadian rhythm regulation. However, its functional roles in oocyte meiosis have not been fully determined. Results We report that CK2 is essential for porcine oocyte meiotic maturation by regulating spindle assembly checkpoint (SAC). Immunostaining and immunoblotting analysis showed that CK2 was constantly expressed and located on the chromosomes during the entire oocyte meiotic maturation. Inhibition of CK2 activity by its selective inhibitor CX-4945 impaired the first polar body extrusion and arrested oocytes at M I stage, accompanied by the presence of BubR1 at kinetochores, indicative of activated SAC. In addition, we found that spindle/chromosome structure was disrupted in CK2-inhibited oocytes due to the weakened microtubule stability, which is a major cause resulting in the activation of SAC. Last, we found that the level DNA damage as assessed by γH2A.X staining was considerably elevated when CK2 was inhibited, suggesting that DNA damage might be another critical factor leading to the SAC activation and meiotic failure of oocytes. Conclusions Our findings demonstrate that CK2 promotes the porcine oocyte maturation by ensuring normal spindle assembly and DNA damage repair.

It has been reported that environmental factors, such as industrial pollution, environmental toxins, environmental hormones, and global warming contribute to the oxidative stress-induced deterioration of oocyte quality and female fertility. However, the prevention or improvement approaches have not been fully elucidated. Here, we explored the mechanism regarding how Mogroside V (MV), a main extract of Siraitia grosvenorii, improves the oxidative stress-induced meiotic defects in porcine oocytes. Our results showed that MV supplementation restores the defective oocyte maturation and cumulus cell expansion caused by H

Individuals of all ages, including children and teenagers, consume 4-methylimidazole (4-MI) in their food. 4-MI is a caramel-colored waste product that has previously been linked to human carcinogenesis and has shown possible signs of reproductive toxicity. This study aimed to determine whether 4-MI is harmful to oocytes during meiosis and fertilization. Female mice were intragastrically administered 0, 50, or 100 mg/kg body weight of 4-MI daily for 10 days. We found that 4-MI affects the quality of oocytes by affecting their meiotic ability and fertility potential. Specifically, 4-MI rendered the meiotic spindles and chromosomes less stable, which halted oocyte maturation and resulted in aneuploidy. 4-MI also slowed the decrease in the levels of cortical granules and their component ovastacin; consequently, sperms could not be bound and fertilization could not occur. We also found that mitochondrial dysfunction was associated with oocytes deterioration. This led to reactive oxygen species accumulation and cell death. Altogether, our findings reveal that the poor condition of oocytes subjected to 4-MI is primarily attributable to mitochondrial malfunction and redox alterations.

Dibutyltin dichloride (DBTCl) is a widespread environmental pollutant that is frequently employed as a light and heat sustainer for polyvinyl chloride (PVC) plastics and is a teratogen in vivo. Nevertheless, its destructiveness in mammalian oocytes remains unclear. This study highlighted the consequences of DBTCl vulnerability on mouse oocyte. Our results revealed that exposure to 5.0 mg/kg/day of DBTCl for ten days reduced the number of mature follicles and oocytes in the ovaries and inhibited the meiotic maturation of oocytes. Single-cell transcriptomic analysis indicated that DBTCl exposure interfered with the expression of more than 400 genes in oocytes, including those involved in multiple biological pathways. Specifically, DBTCl exposure impaired spindle assembly and chromosome alignment. In addition, DBTCl exposure caused mitochondrial dysfunction, which led to the accumulation of reactive oxygen species (ROS) and induced apoptosis. In summary, our study illustrates that mitochondrial dysfunction and redox perturbation are the major causes of the reduced quality of oocytes exposed to DBTCl.

Objectives Histone deacetylase 8 (HDAC8) is one of the class I HDAC family proteins, which participates in the neuronal disorders, parasitic/viral infections, tumorigenesis and many other biological processes. However, its potential function during female germ cell development has not yet been fully understood. Materials and methods HDAC8‐targeting siRNA was microinjected into GV oocytes to deplete HDAC8. PCI‐34051 was used to inhibit the enzyme activity of HDAC8. Immunostaining, immunoblotting and fluorescence intensity quantification were applied to assess the effects of HDAC8 depletion or inhibition on the oocyte meiotic maturation, spindle/chromosome structure, γ‐tubulin dynamics and acetylation level of α‐tubulin. Results We observed that HDAC8 was localized in the nucleus at GV stage and then translocated to the spindle apparatus from GVBD to M II stages in porcine oocytes. Depletion of HDAC8 led to the oocyte meiotic failure by showing the reduced polar body extrusion rate. In addition, depletion of HDAC8 resulted in aberrant spindle morphologies and misaligned chromosomes due to the defective recruitment of γ‐tubulin to the spindle poles. Notably, these meiotic defects were photocopied by inhibition of HDAC8 activity using its specific inhibitor PCI‐34051. However, inhibition of HDAC8 did not affect microtubule stability as assessed by the acetylation level of α‐tubulin. Conclusions Collectively, our findings demonstrate that HDAC8 acts as a regulator of spindle assembly during porcine oocyte meiotic maturation., Our findings document that HDAC8 locates to the spindle apparatus in porcine oocytes to take part in the spindle assembly via recruitment of γ‐tubulin to the spindle poles, and hence driving the oocyte meiotic maturation. This function of HDAC8 relies on its enzyme activity and is conserved among species in mammals.

Video retrieval is becoming increasingly important owing to the rapid emergence of videos on the Internet. The dominant paradigm for video retrieval learns video-text representations by pushing the distance between the similarity of positive pairs and that of negative pairs apart from a fixed margin. However, negative pairs used for training are sampled randomly, which indicates that the semantics between negative pairs may be related or even equivalent, while most methods still enforce dissimilar representations to decrease their similarity. This phenomenon leads to inaccurate supervision and poor performance in learning video-text representations. While most video retrieval methods overlook that phenomenon, we propose an adaptive margin changed with the distance between positive and negative pairs to solve the aforementioned issue. First, we design the calculation framework of the adaptive margin, including the method of distance measurement and the function between the distance and the margin. Then, we explore a novel implementation called "Cross-Modal Generalized Self-Distillation" (CMGSD), which can be built on the top of most video retrieval models with few modifications. Notably, CMGSD adds few computational overheads at train time and adds no computational overhead at test time. Experimental results on three widely used datasets demonstrate that the proposed method can yield significantly better performance than the corresponding backbone model, and it outperforms state-of-the-art methods by a large margin., Comment: Accepted by SIGIR 2021

Age-related decline in female fertility is a common feature that occurs in the fourth decade of women as a result of a reduction in both oocyte quality and quantity [1]. However, strategies to prevent the deterioration of maternal aged oocytes and relevant mechanisms are still underexplored. Here, we find that the reduced abundance of melatonin in the follicular fluid highly correlates with the advanced maternal age-related aneuploidy. Of note, we show that exposure of oocytes from aged mice both in vitro and in vivo to exogenous melatonin not only eliminates the accumulated reactive oxygen species-induced DNA damage and apoptosis, but also suppresses the occurrence of aneuploidy caused by spindle/chromosome defect that is frequently observed in aged oocytes. Importantly, we reveal that melatonin supplementation reverses the defective phenotypes in aged oocytes through a Sirt1/Sod2-dependent mechanism. Inhibition of Sirt1 activity abolishes the melatonin-mediated improvement of aged oocyte quality. Together our findings provide evidence that supplementation of melatonin is a feasible way to protect oocytes from advanced maternal age-related meiotic defects and aneuploidy, demonstrating the potential for improving the quality of oocytes from aged women and the efficiency of assisted reproductive technology., Graphical abstract Image 1, Highlights • Melatonin abundance in the follicular fluid declines with age in the mouse. • In vitro treatment of aged oocytes with melatonin eliminates the excessive ROS and reduces the occurrence of aneuploidy. • In vivo administration of advanced-age mice with melatonin protects oocytes from spindle/chromosome defects and aneuploidy. • Melatonin supplementation reverses the meiotic defects in aged oocytes through activation of Sirt1/Sod2 pathway.

STUDY QUESTION Does melatonin restore the benzo(a)pyrene (BaP)-induced meiotic failure in porcine oocytes? SUMMARY ANSWER Melatonin effectively inhibits the increased reactive oxygen species (ROS) level and apoptotic rate in BaP-exposed porcine oocytes to recover the meiotic failure. WHAT IS KNOWN ALREADY BaP, a widespread environmental carcinogen found in particulate matter, 2.5 µm or less (PM2.5), has been shown to have toxicity at the level of the reproductive systems. BaP exposure disrupts the steroid balance, alters the expression of ovarian estrogen receptor and causes premature ovarian failure through the rapid depletion of the primordial follicle pool. In addition, acute exposure to BaP has transient adverse effects on the follicle growth, ovulation and formation of corpora lutea, which results in transient infertility. STUDY DESIGN, SIZE, DURATION Porcine oocytes were randomly assigned to control, BaP-exposed and melatonin-supplemented groups. BaP was dissolved in dimethylsulphoxide and diluted to a final concentration of 50, 100 or 250 μM with maturation medium, respectively. Melatonin was dissolved in the absolute ethanol and diluted with maturation medium to a final concentration of 1 nM, 100 nM, 10 μM and 1 mM, respectively. The in vitro cultured oocytes from each group after treatment were applied to the subsequent analysis. PARTICIPANTS/MATERIALS, SETTING, METHODS Acquisition of oocyte meiotic competence was assessed using immunostaining, fluorescent intensity quantification and/or immunoblotting to analyse the cytoskeleton assembly, mitochondrial integrity, cortical granule dynamics, ovastacin distribution, ROS level and apoptotic rate. Fertilization ability of oocytes was examined by sperm binding assay and IVF. MAIN RESULTS AND THE ROLE OF CHANCE BaP exposure resulted in the oocyte meiotic failure (P = 0.001) via impairing the meiotic apparatus, showing a prominently defective spindle assembly (P = 0.003), actin dynamics (P < 0.001) and mitochondrion integrity (P < 0.001). In addition, BaP exposure caused the abnormal distribution of cortical granules (P < 0.001) and ovastacin (P = 0.003), which were consistent with the observation that fewer sperm bound to the zona pellucida surrounding the unfertilized BaP-exposed eggs (P < 0.001), contributing to the fertilization failure (P < 0.001). Conversely, melatonin supplementation recovered, at least partially, all the meiotic defects caused by BaP exposure through inhibiting the rise in ROS level (P = 0.015) and apoptotic rate (P = 0.001). LIMITATIONS, REASONS FOR CAUTION We investigated the negative impact of BaP on the oocyte meiotic maturation in vitro, but not in vivo. WIDER IMPLICATIONS OF THE FINDINGS Our findings not only deeply clarify the potential mechanisms of BaP-induced oocyte meiotic failure, but also extend the understanding about how environmental pollutants influence the reproductive systems in humans. STUDY FUNDING/COMPETING INTERESTS This study was supported by the National Natural Science Foundation of China (31571545) and the Natural Science Foundation of Jiangsu Province (BK20150677). The authors have no conflict of interest to disclose.

Sister chromatid cohesion, mediated by cohesin complex and established by the acetyltransferases Esco1 and Esco2, is essential for faithful chromosome segregation. Mutations in Esco2 cause Roberts syndrome, a developmental disease characterized by severe prenatal retardation as well as limb and facial abnormalities. However, its exact roles during oocyte meiosis have not clearly defined. Here, we report that Esco2 localizes to the chromosomes during oocyte meiotic maturation. Depletion of Esco2 by morpholino microinjection leads to the precocious polar body extrusion, the escape of metaphase I arrest induced by nocodazole treatment and the loss of BubR1 from kinetochores, indicative of inactivated SAC. Furthermore, depletion of Esco2 causes a severely impaired spindle assembly and chromosome alignment, accompanied by the remarkably elevated incidence of defective kinetochore-microtubule attachments which consequently lead to the generation of aneuploid eggs. Notably, we find that the involvement of Esco2 in SAC and kinetochore functions is mediated by its binding to histone H4 and acetylation of H4K16 both in vivo and in vitro. Thus, our data assign a novel meiotic function to Esco2 beyond its role in the cohesion establishment during mouse oocyte meiosis.

Smc1β is a meiosis-specific cohesin subunit that is essential for sister chromatid cohesion and DNA recombination. Previous studies have shown that Smc1β-deficient mice in both sexes are sterile. Ablation of Smc1β during male meiosis leads to the blockage of spermatogenesis in pachytene stage, and ablation of Smc1β during female meiosis generates a highly error-prone oocyte although it could develop to metaphase II stage. However, the underlying mechanisms regarding how Smc1β maintains the correct meiotic progression in mouse oocytes have not been clearly defined. Here, we find that GFP-fused Smc1β is expressed and localized to the chromosomes from GV to MII stages during mouse oocyte meiotic maturation. Knockdown of Smc1β by microinjection of gene-specific morpholino causes the impaired spindle apparatus and chromosome alignment which are highly correlated with the defective kinetochore-microtubule attachments, consequently resulting in a prominently higher incidence of aneuploid eggs. In addition, the premature extrusion of polar bodies and escape of metaphase I arrest induced by low dose of nocodazole treatment in Smc1β-depleted oocytes indicates that Smc1β is essential for activation of spindle assembly checkpoint (SAC) activity. Collectively, we identify a novel function of Smc1β as a SAC participant beyond its role in chromosome cohesion during mouse oocyte meiosis.

HDAC8 is a class I histone deacetylase that functions in a variety of biological processes through its non-histone substrates. However, its roles during oocyte meiosis remain elusive. Here, we document that HDAC8 localizes at spindle poles and positively participates in the regulation of microtubule organization and spindle assembly in mouse oocytes. Depletion of HDAC8 by siRNA-based gene silencing results in various spindle defects and chromosome misalignment during oocyte meiotic maturation, accompanied by impaired kinetochore-microtubule attachments. Consequently, a higher incidence of aneuploidy is generated in HDAC8-depleted MII eggs. In addition, inhibition of HDAC8 activity with its selective inhibitor PCI-34051 phenocopies the spindle/chromosome defects resulting from HDAC8 depletion by siRNA injection. Finally, we find that HDAC8 is required for the correct localization of I•-tubulin to spindle poles. Collectively, these data reveal that HDAC8 plays a significant role in regulating spindle assembly and thus ensuring the euploidy in mouse eggs.

In mammalian cells, cohesin acetyltransferases Esco1 and Esco2 acetylate cohesin subunit Smc3 to establish chromosome cohesion, ensuring the accurate chromosome segregation. However, we have previously documented that both Esco1 and Esco2 have unique substrates and roles in mouse oocyte meiosis I to orchestrate the meiotic progression, but whether these functions are conserved among species is still not determined. Here, we used porcine oocytes as a model to illustrate that Esco1 and Esco2 exerted conserved functions during oocyte meiosis. We observed that Esco1 and Esco2 exhibited different localization patterns in porcine oocytes. Esco1 was localized to the spindle apparatus while Esco2 was distributed on the chromosomes. Depletion of Esco1 by siRNA microinjection caused the meiotic arrest by showing the reduced frequency of first polar body extrusion and defective spindle/chromosome structure. In addition, Esco1 bound to α-tubulin and was required for its acetylation level to maintain the microtubule dynamics. By contrast, depletion of Esco2 by siRNA microinjection resulted in the accelerated meiotic progression by displaying the precocious polar body extrusion and inactivation of spindle assembly checkpoint. Notably, Esco2 was shown to be associated with histone H4 for the acetylation of H4K16 to modulate the kinetochore function. Collectively, our data reveal that Esco1 and Esco2 perform distinct and conserved functions in oocytes to drive the meiotic progression beyond their canonical roles in the cohesion establishment.

// Mianqun Zhang 1 , Xiaoxin Dai 1 , Yalu Sun 1 , Yajuan Lu 1 , Changyin Zhou 1 , Yilong Miao 1 , Ying Wang 2 , Bo Xiong 1 1 College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China 2 Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China Correspondence to: Bo Xiong, email: xiongbo@njau.edu.cn Keywords: Stag3, spindle assembly, chromosome alignment, microtubule stability, aneuploid egg Received: October 20, 2016 Accepted: November 12, 2016 Published: November 29, 2016 ABSTRACT Stag3, a meiosis-specific subunit of cohesin complex, has been demonstrated to function in both male and female reproductive systems in mammals. However, its roles during oocyte meiotic maturation have not been fully defined. In the present study, we report that Stag3 uniquely accumulates on the spindle apparatus and colocalizes with microtubule fibers during mouse oocyte meiotic maturation. Depletion of Stag3 by gene-targeting morpholino disrupts normal spindle assembly and chromosome alignment in oocytes. We also find that depletion of Stag3 reduces the acetylated level of tubulin and microtubule resistance to microtubule depolymerizing drug, suggesting that Stag3 is required for microtubule stability. Consistent with these observations, kinetochore-microtubule attachment, an important mechanism controlling chromosome alignment, is severely impaired in Stag3-depleted oocytes, resultantly causing the significantly increased incidence of aneuploid eggs. Collectively, our data reveal that Stag3 is a novel regulator of microtubule dynamics to ensure euploidy during moue oocyte meiotic maturation.

This paper is concerned with bounded synchronization for a class of the complex dynamical network with delay feedback controller. In order to realize bounded synchronization of complex networks, several new inequality theorems are proposed, and bounded synchronization criteria of complex dynamical networks are also derived based on inequality theorems. Finally, two numerical examples are provided to verify the theoretical results established in this paper.

Negative effects of postovulatory aging on fertilization ability and subsequent embryo development have been reported in rodents; however, the molecular and cellular changes during this process have not been fully defined. Here, we used porcine oocytes, a model that is physiologically and developmentally similar to humans, to explore the molecular mechanisms that underlie how postovulatory aging affects oocyte quality and fertilization capacity. We found that postovulatory aging caused the morphologic change of porcine oocytes by exhibiting the incompact expansion of cumulus cells and an increased occurrence of fragmentation. Aging also impaired oocyte quality by disrupting organelle structures, including the spindle assembly, actin polymerization, and mitochondrial integrity. Moreover, postovulatory aging led to the abnormal distribution of cortical granules and ovastacin, which, in turn, resulted in defective sperm binding and consequently compromised fertilization potential. Of note, we observed that postovulatory aging induced oxidative stress with a high level of reactive oxygen species and apoptotic rate in oocytes, thereby resulting in the deterioration of critical factors in the maintenance of oocyte quality and fertilization capacity. Taken together, our findings demonstrate that postovulatory aging perturbs a variety of molecular and cellular changes in porcine oocytes by inducing oxidative stress.-Miao, Y., Zhou, C., Cui, Z., Zhang, M., ShiYang, X., Lu, Y., Xiong, B. Postovulatory aging causes the deterioration of porcine oocytes via induction of oxidative stress.

Cytoplasmic dynein is a family of cytoskeletal motor proteins that move towards the minus-end of the microtubules to perform functions in a variety of mitotic processes such as cargo transport, organelle positioning, chromosome movement and centrosome assembly. However, its specific roles during mammalian oocyte meiosis have not been fully defined. Herein, we investigated the critical events during porcine oocyte meiotic maturation after inhibition of dynein by Ciliobrevin D treatment. We found that oocyte meiotic progression was arrested when inhibited of dynein by showing the poor expansion of cumulus cells and decreased rate of polar body extrusion. Meanwhile, the spindle assembly and chromosome alignment were disrupted, accompanied by the reduced level of acetylated α-tubulin, indicative of weakened microtubule stability. Defective actin polymerization on the plasma membrane was also observed in dynein-inhibited oocytes. In addition, inhibition of dynein caused the abnormal distribution of cortical granules and precocious exocytosis of ovastacin, a cortical granule component, which predicts that ZP2, the sperm binding site in the zona pellucida, might be prematurely cleaved in the unfertilized dynein-inhibited oocytes, potentially leading to the fertilization failure. Collectively, our findings reveal that dynein plays a part in porcine oocyte meiotic progression by regulating the cytoskeleton dynamics including microtubule stability, spindle assembly, chromosome alignment and actin polymerization. We also find that dynein mediates the normal cortical granule distribution and exocytosis timing of ovastacin in unfertilized eggs which are the essential for the successful fertilization.

Esco1 has been reported to function as a cohesion establishment factor that mediates chromosome cohesion and segregation in mitotic cells. However, its exact roles in meiosis have not been clearly defined. Here, we document that Esco1 is expressed and localized to both the nucleus and cytoplasm during mouse oocyte meiotic maturation. Depletion of Esco1 by siRNA microinjection causes the meiotic progression arrest with a severe spindle abnormality and chromosome misalignment, which is coupled with a higher incidence of the erroneous kinetochore–microtubule attachments and activation of spindle assembly checkpoint. In addition, depletion of Esco1 leads to the impaired microtubule stability shown by the weakened resistance ability to the microtubule depolymerizing drug nocodazole and the decreased level of acetylated α-tubulin. Conversely, overexpression of Esco1 causes hyperacetylation of α-tubulin and spindle defects. Moreover, we find that Esco1 binds to α-tubulin and is required for its acetylation. The reduced acetylation level of α-tubulin in Esco1-depleted oocytes can be restored by the ectopic expression of exogenous wild-type Esco1 but not enzymatically dead Esco1-G768D. Purified wild-type Esco1 instead of mutant Esco1-G768D acetylates the synthesized peptide of α-tubulin in vitro. Collectively, our data assign a novel function to Esco1 as a microtubule regulator during oocyte meiotic maturation beyond its conventional role in chromosome cohesion.

Benzo[a]pyrene (BaP) is a ubiquitous environmental pollutant and carcinogen that is frequently found in particulate matter, with a diameter of ≤2.5 μm (PM2.5). It has been reported to interrupt the normal reproductive system, but the exact molecular basis has not been clearly defined. To understand the underlying mechanisms regarding how BaP exposure disrupts female fertility, we evaluated oocyte quality by assessing the critical regulators and events during oocyte meiotic maturation and fertilization. We found that BaP exposure compromised the mouse oocyte meiotic progression by disrupting normal spindle assembly, chromosome alignment, and kinetochore-microtubule attachment, consequently leading to the generation of aneuploid eggs. In addition, BaP administration significantly decreased the fertilization rate of mouse eggs by reducing the number of sperm binding to the zona pellucida, which was consistent with the premature cleavage of N terminus of zona pellucida sperm-binding protein 2 and precocious exocytosis of ovastacin. Furthermore, BaP exposure interfered with the gamete fusion process by perturbing the localization and protein level of Juno. Notably, we found that BaP exposure induced oxidative stress with an increased level of reactive oxygen species and apoptosis in oocytes and thereby led to the deterioration of critical regulators and events during oocyte meiotic progression and fertilization. Our data document that BaP exposure reduces female fertility via impairing oocyte maturation and fertilization ability induced by oxidative stress and early apoptosis in murine models.-Zhang, M., Miao, Y., Chen, Q., Cai, M., Dong, W., Dai, X., Lu, Y., Zhou, C., Cui, Z., Xiong, B. BaP exposure causes oocyte meiotic arrest and fertilization failure to weaken female fertility.

Study question What are the underlying mechanisms of the decline in the fertilization ability of post-ovulatory aged oocytes? Summary answer Melatonin improves the fertilization ability of post-ovulatory aged oocytes by reducing aging-induced reactive oxygen species (ROS) levels and inhibiting apoptosis and by maintaining the levels and localization of the fertilization proteins, ovastacin and Juno. What is known already Following ovulation, the quality of mammalian metaphase II oocytes irreversibly deteriorates over time with a concomitant loss of fertilization ability. Melatonin has been found to prevent post-ovulatory oocyte aging and extend the window for optimal fertilization in mice. Study design, size, duration Mouse oocytes were randomly assigned to three groups and aged in vitro for 0, 6, 12 and 24 h, respectively. Increasing concentrations of melatonin (10-9 M, 10-7 M, 10-5 M and 10-3 M) were added to the 24 h aging group. Participants/materials, setting, methods Sperm binding assays, in-vitro fertilization, immunofluorescent staining and western blotting were performed to investigate key regulators and events during fertilization of post-ovulatory aged mouse oocytes. Main results and the role of chance We found that the actin cap which promotes a cortical granule (CG) free domain is disrupted with a re-distribution of CGs in the subcortex of aged oocytes. Ovastacin, a CG metalloendoprotease, is mis-located and prematurely exocytosed in aged oocytes with subsequent cleavage of the zona pellucida protein ZP2. This disrupts the sperm recognition domain and dramatically reduces the number of sperm binding to the zona pellucida. The abundance of Juno, the sperm receptor on the oocyte membrane, also is reduced in aged oocytes. Exposure of aged oocytes to melatonin significantly elevates in-vitro fertilization rates potentially by rescuing the above age-associated defects of fertilization, and reducing ROS and inhibiting apoptosis. Large scale data N/A. Limitations, reasons for caution We explored the mechanisms of the decline in fertilization ability decline in aged mouse oocytes, in vitro but not in vivo. Wider implications of the findings Our findings may contribute to the development a more efficient method, involving melatonin, for improving IVF success rates. Study funding/competing interest(s) This study was supported by the National Natural Science Foundation (31571545) and the Natural Science Foundation of Jiangsu Province (BK20150677). The authors have no conflict of interest to disclose.

The Cullin9 gene encodes a putative E3 ligase that serves a wide variety of biological functions in mitosis, whereas its roles in meiosis have not yet clearly defined. Here, we report that Cullin9 accumulates on the spindle apparatus and colocalizes with the microtubule fibers during mouse oocyte meiotic maturation. Depletion of Cullin9 by morpholino microinjection results in a remarkably higher rate of disorganized spindles and misaligned chromosomes in oocytes, which is coupled with the impaired kinetochore-microtubule attachments. Resultantly, the incidence of aneuploid eggs significantly increases in Cullin9-depleted oocytes. Moreover, we show that Cullin9 controls Survivin's protein level during meiotic maturation, and thus regulates microtubule stability in oocytes. Thus, our study assigns a new meiotic function to Cullin9 and reveals that it prevents mouse eggs from aneuploidy by regulating microtubule dynamics via Survivin.

Bisphenol A (BPA) has been reported to adversely affect the mammalian reproductive system in both sexes. However, the underlying mechanisms regarding how BPA disrupts the mammalian oocyte quality and how to prevent it have not been fully defined. Here, we document that BPA weakens oocyte quality by impairing both oocyte meiotic maturation and fertilization ability. We find that oral administration of BPA (100 μg/kg body weight per day for 7 days) compromises the first polar body extrusion (78.0% vs 57.0%, P

This paper examines the VaRs of daily stock market returns before and after the introduction of stock indexfutures contract trading in China from a statistical perspective. VaRs, in this paper, are estimated with peaks overthreshold (POT) method fitting the tails of data distributions well. The key empirical results show that the VaRsof daily returns before stock index futures are greater than those after the stock index futures at the samesignificance levels. The market risk of Chinese stock market decreased after the introduction of stock indexfutures.

Melamine is an organic nitrogenous compound widely used as an industrial chemical, and it has been recently reported by us that melamine has a toxic effect on the female reproductive system in mice, and renders females subfertile; the molecular basis, however, has not been adequately assessed. In the present study, we explore the underlying mechanism regarding how melamine compromises fertility in the mouse. The data showed that melamine exposure significantly impaired the fertilization capability of the egg during in vitro fertilization. To further figure out the cause, we analyzed ovastacin localization and protein level, the sperm binding ability of zona pellucida, and ZP2 cleavage status in unfertilized eggs from melamine fed mice, and no obvious differences were found between control and treatment groups. However, the protein level of Juno on the egg plasma membrane in the high-dose feeding group indeed significantly decreased compared to the control group. Thus, these data suggest that melamine compromises female fertility via suppressing Juno protein level on the egg membrane.

This paper investigated the dominant species of insect communities in five stored export products along Yangtze River in Jiangsu Province. With the indexes species richness, ecological dominance, community diversity and evenness, the numerical characteristics of insect community structure in the stored products were analyzed, and the similarity of the communities was also analyzed. By the method of hierarchical cluster analysis, the numerical classification was made, and the communities were grouped into 4 groups. The insect communities in stored willow and feather products were in the same group, while those in other stored products were grouped into 3 groups. Except that in woodwork products, the insect community structures in other stored products, especially in leather products, were not rational.