CaMKII autophosphorylation is the only enzymatic event required for synaptic memory.

Ca2+/calmodulin (CaM)-dependent kinase II (CaMKII) plays a critical role in long-term potentiation (LTP), a well-established model for learning and memory through the enhancement of synaptic transmission. Biochemical studies indicate that CaMKII catalyzes a phosphotransferase (kinase) reaction of both itself (autophosphorylation) and of multiple downstream target proteins. However, whether either type of phosphorylation plays any role in the synaptic enhancing action of CaMKII remains hotly contested. We have designed a series of experiments to define the minimal requirements for the synaptic enhancement by CaMKII. We find that autophosphorylation of T286 and further binding of CaMKII to the GluN2B subunit are required both for initiating LTP and for its maintenance (synaptic memory). Once bound to the NMDA receptor, the synaptic action of CaMKII occurs in the absence of target protein phosphorylation. Thus, autophosphorylation and binding to the GluN2B subunit are the only two requirements for CaMKII in synaptic memory.

Single-Cell Analysis in Blood Reveals Distinct Immune Cell Profiles in Gouty Arthritis.

Gout is a chronic disease caused by monosodium urate crystal deposition. Previous studies have focused on the resident macrophage, infiltrating monocyte, and neutrophil responses to monosodium urate crystal, yet the mechanisms of the potential involvement of other immune cells remain largely unknown. In this study, we enrolled seven gout patients and five age-matched healthy individuals and applied single-cell mass cytometry to study the distribution of immune cell subsets in peripheral blood. To our knowledge, our study reveals the immune cell profiles of gout at different stages for the first time. We identified many immune cell subsets that are dysregulated in gout and promote gouty inflammation, especially those highly expressing CCR4 and OX40 (TNFR superfamily member 4), including CCR4+OX40+ monocytes, CCR4+OX40+CD56high NK cells, CCR4+OX40+CD4+ NK T cells, and CCR4+CD38+CD4+ naïve T cells. Notably, the plasma levels of CCL17 and CCL22, measured by ELISA, increased in the acute phase of gout and declined in the interval. We also found a clue that Th2-type immune responses may participate in gout pathology. Moreover, the subset of granzyme B+ (GZMB+) CD38+ NK cells is positively correlated with serum urea acid level, and another two γδT subsets, GZMB+CD161+ γδT cells and GZMB+CCR5+ γδT cells, are negatively correlated with erythrocyte sedimentation rate. In sum, gouty arthritis is not a disease simply mediated by macrophages; multiple types of immune cell may be involved in the pathogenesis of the disease. Future research needs to shift attention to other immune cell subsets, such as NK cells and T cells, which will facilitate the identification of novel therapeutic targets.

Synaptic memory survives molecular turnover.

Activation of Ca2+/calmodulin-dependent kinase II (CaMKII) plays a critical role in long-term potentiation (LTP), a long accepted cellular model for learning and memory. However, how LTP and memories survive the turnover of synaptic proteins, particularly CaMKII, remains a mystery. Here, we take advantage of the finding that constitutive Ca2+-independent CaMKII activity, acquired prior to slice preparation, provides a lasting memory trace at synapses. In slice culture, this persistent CaMKII activity, in the absence of Ca2+ stimulation, remains stable over a 2-wk period, well beyond the turnover of CaMKII protein. We propose that the nascent CaMKII protein present at 2 wk acquired its activity from preexisting active CaMKII molecules, which transferred their activity to newly synthesized CaMKII molecules and thus maintain the memory in the face of protein turnover.

MAGUKs are essential, but redundant, in long-term potentiation.

This study presents evidence that the MAGUK family of synaptic scaffolding proteins plays an essential, but redundant, role in long-term potentiation (LTP). The action of PSD-95, but not that of SAP102, requires the binding to the transsynaptic adhesion protein ADAM22, which is required for nanocolumn stabilization. Based on these and previous results, we propose a two-step process in the recruitment of AMPARs during LTP. First, AMPARs, via TARPs, bind to exposed PSD-95 in the PSD. This alone is not adequate to enhance synaptic transmission. Second, the AMPAR/TARP/PSD-95 complex is stabilized in the nanocolumn by binding to ADAM22. A second, ADAM22-independent pathway is proposed for SAP102.

LGI1-ADAM22-MAGUK configures transsynaptic nanoalignment for synaptic transmission and epilepsy prevention.

Physiological functioning and homeostasis of the brain rely on finely tuned synaptic transmission, which involves nanoscale alignment between presynaptic neurotransmitter-release machinery and postsynaptic receptors. However, the molecular identity and physiological significance of transsynaptic nanoalignment remain incompletely understood. Here, we report that epilepsy gene products, a secreted protein LGI1 and its receptor ADAM22, govern transsynaptic nanoalignment to prevent epilepsy. We found that LGI1-ADAM22 instructs PSD-95 family membrane-associated guanylate kinases (MAGUKs) to organize transsynaptic protein networks, including NMDA/AMPA receptors, Kv1 channels, and LRRTM4-Neurexin adhesion molecules. Adam22ΔC5/ΔC5 knock-in mice devoid of the ADAM22-MAGUK interaction display lethal epilepsy of hippocampal origin, representing the mouse model for ADAM22-related epileptic encephalopathy. This model shows less-condensed PSD-95 nanodomains, disordered transsynaptic nanoalignment, and decreased excitatory synaptic transmission in the hippocampus. Strikingly, without ADAM22 binding, PSD-95 cannot potentiate AMPA receptor-mediated synaptic transmission. Furthermore, forced coexpression of ADAM22 and PSD-95 reconstitutes nano-condensates in nonneuronal cells. Collectively, this study reveals LGI1-ADAM22-MAGUK as an essential component of transsynaptic nanoarchitecture for precise synaptic transmission and epilepsy prevention.

The evolution of ancestral and species-specific adaptations in snowfinches at the Qinghai-Tibet Plateau.

Species in a shared environment tend to evolve similar adaptations under the influence of their phylogenetic context. Using snowfinches, a monophyletic group of passerine birds (Passeridae), we study the relative roles of ancestral and species-specific adaptations to an extreme high-elevation environment, the Qinghai-Tibet Plateau. Our ancestral trait reconstruction shows that the ancestral snowfinch occupied high elevations and had a larger body mass than most nonsnowfinches in Passeridae. Subsequently, this phenotypic adaptation diversified in the descendant species. By comparing high-quality genomes from representatives of the three phylogenetic lineages, we find that about 95% of genes under positive selection in the descendant species are different from those in the ancestor. Consistently, the biological functions enriched for these species differ from those of their ancestor to various degrees (semantic similarity values ranging from 0.27 to 0.5), suggesting that the three descendant species have evolved divergently from the initial adaptation in their common ancestor. Using a functional assay to a highly selective gene, DTL, we demonstrate that the nonsynonymous substitutions in the ancestor and descendant species have improved the repair capacity of ultraviolet-induced DNA damage. The repair kinetics of the DTL gene shows a twofold to fourfold variation across the ancestor and the descendants. Collectively, this study reveals an exceptional case of adaptive evolution to high-elevation environments, an evolutionary process with an initial adaptation in the common ancestor followed by adaptive diversification of the descendant species.

Study on the behavior of clusters in the physical recovery of GaAs scrap.

Gallium arsenide (GaAs) is the most widely used second-generation semiconductor material. However, a large amount of GaAs scrap is generated at various stages of the GaAs wafer production process. Volatile GaAs clusters are inevitably generated during the process of GaAs vacuum thermal decomposition, resulting in lower purity of the recovered arsenic and the loss of gallium. In this study, thermodynamic analysis and dynamics simulation were combined to discuss the possibility of separating GaAs clusters and arsenic from a microscopic perspective. A vacuum thermal decomposition-directional condensation recovery process for GaAs scrap was proposed. By properly adjusting the separation parameters such as heating temperature, holding time and raw material size, high purity of gallium (99.99%) and arsenic (99.5%) were directly recovered under a system pressure of 1 Pa, heating temperature of 1323 K, holding time of 3 h, and GaAs scrap size of 2.5 cm. GaAs clusters were also recovered in powder form. The problem of difficult separation of GaAs clusters from arsenic was effectively solved by this method, and the purity of recovered arsenic was greatly improved. No additives are required and no waste liquid or gas emission in the whole process. The complexity of subsequent arsenic purification operations and the threat of arsenic containing waste to the environment were reduced as well.

Insights into the cellular, molecular, and epigenetic targets of gamma-aminobutyric acid against diabetes: a comprehensive review on its mechanisms.

Diabetes is a metabolic disease due to impaired or defective insulin secretion and is considered one of the most serious chronic diseases worldwide. Gamma-aminobutyric acid (GABA) is a naturally occurring non-protein amino acid commonly present in a wide range of foods. A number of studies documented that GABA has good anti-diabetic potential. This review summarized the available dietary sources of GABA as well as animal and human studies on the anti-diabetic properties of GABA, while also discussing the underlying mechanisms. GABA may modulate diabetes through various pathways such as inhibiting the activities of α-amylase and α-glucosidase, promoting ß-cell proliferation, stimulating insulin secretion from ß-cells, inhibiting glucagon secretion from α-cells, improving insulin resistance and glucose tolerance, and increasing antioxidant and anti-inflammatory activities. However, further mechanistic studies on animals and human are needed to confirm the therapeutic effects of GABA against diabetes.

Mangiferin: a review of dietary sources, absorption, metabolism, bioavailability, and safety.

Mangiferin is a potential candidate for use in nutraceutical and functional food applications due to its numerous bioactivities. However, the low bioavailability of mangiferin is a major limitation for establishing efficacy for use. This review describes current information on known food sources and factors that influence mangiferin contents, absorption, and metabolism features, and recent progress that has come from research efforts to increase the bioavailability of mangiferin. We also list patents that targeted to enhance mangiferin bioavailability. Mangifera indica L. is the major dietary source for mangiferin, a xanthone that varies widely in different parts of the plant and is influenced by many factors that involve plant propagation and post-harvest processing. Mangiferin absorption occurs mostly in the small intestine by passive diffusion with varying absorption capacities in different segments of the gastrointestinal tract. Recent research has led to the development of novel technologies to encapsulate mangiferin in nano/microparticle carrier systems as well as generate mangiferin derivatives to improve solubility and bioavailability. Preclinical studies reported that mangiferin < 2000 mg/kg is generally nontoxic. The safety and the increase in bioavailability are key limiting factors for developing successful applications for mangiferin as a nutritional dietary supplement or nutraceutical.Supplemental data for this article is available online at.

Selective sulfidation-vacuum volatilization processes for tellurium and bismuth recovery from bismuth telluride waste thermoelectric material.

Bismuth telluride-based alloy materials are currently the best performing thermoelectric materials at near room temperature; however, their production and use generate waste (e.g., cutting waste and failed grains). There is also lack of efficient recycling strategies for the generated waste. In this study, a selective sulfidation-vacuum volatilization method is proposed for recovering bismuth telluride waste. The Gibbs free energies of the sulfidation reaction of bismuth telluride are calculated, the saturated vapor pressure of each substance is analyzed, and the composition of the products is predicted. Based on the differences among the sulfidation and volatile properties of bismuth and tellurium, by adding sulfur to bismuth telluride waste, the composition of the substances was regulated, and efficient separation of tellurium and bismuth was achieved. We combined theoretical calculations and experimental studies to investigate the effect of process conditions on the separation and recovery of tellurium and bismuth. The results show that bismuth was thoroughly sulfereted and tellurium was a pure metal when the mass ratio of sulfur to bismuth telluride was 0.168, the sulfidation temperature was 573 K, and the holding time was 60 min. After sulfidation of the bismuth telluride waste, the sulfides were telluride and bismuthous sulfide. The sulfides, that resulted from sulfureted bismuth telluride production, were treated via vacuum volatilization. The optimal vacuum volatilization condition was 873 K for 120 min. The purities of tellurium and bismuth sulfide obtained by the selective sulfidation-vacuum volatilization experiment were >99%. The distribution ratios of tellurium and bismuth were 98.46% and 99.59%, respectively. The method thoroughly separated tellurium and bismuth from bismuth telluride waste, considerably reducing the environmental and economic costs compared with those of the conventional processes.

Multispectroscopic and Computational Investigations on the Binding Mechanism of Dicaffeoylquinic Acids with Ovalbumin.

Recently, studies on the interactions between ovalbumin (OVA) and polyphenols have received a great deal of interest. This study explored the conformational changes and the interaction mechanism of the binding between OVA and chlorogenic acid (CGA) isomers such as 3,4-dicaffeoylquinic acids (3,4-diCQA), 4,5-dicaffeoylquinic acids (4,5-diCQA), and 3,5-dicaffeoylquinic acids (3,5-diCQA) using multispectroscopic and in silico analyses. The emission spectra show that the diCQAs caused strong quenching of OVA fluorescence under different temperatures through a static quenching mechanism with hydrogen bond (H-bond) and van der Waals (vdW) interactions. The values of binding constants (OVA-3,4-diCQA = 6.123 × 105, OVA-3,5-diCQA = 2.485 × 105, OVA-4,5-diCQA = 4.698 × 105 dm3 mol-1 at 298 K) suggested that diCQAs had a strong binding affinity toward OVA, among which OVA-3,4-diCQA exhibits higher binding constant. The results of UV-vis absorption and synchronous fluorescence indicated that the binding of all three diCQAs to OVA induced conformational and micro-environmental changes in the protein. The findings of molecular modeling further validate the significant role of vdW force and H-bond interactions in ensuring the stable binding of OVA-diCQA complexes. Temperature-dependent molecular dynamics simulation studies allow estimation of the individual components that contribute to the total bound free energy value, which allows evaluation of the nature of the interactions involved. This research can provide information for future investigations on food proteins' physicochemical stability and CGA bioavailability in vitro or in vivo.

Structural, electronic and catalytic properties of AgnSnn (n = 2-14) clusters by density functional theory.

Density functional theory (DFT) calculations of clusters were carried out to investigate the structural and electronic properties of AgnSnn (n = 2-14) clusters. Their lowest energy structure, average binding energy, second-order differential energy, HOMO-LUMO energy gap and density of states were analyzed. The reactions of carbon monoxide and oxygen on the Ag8 cluster and Ag4Sn4 cluster were compared to measure the adsorption and catalytic properties of the Ag4Sn4 cluster. The results show that Ag atoms gather together and are encapsulated by peripheral Sn atoms. The Ag4Sn4 cluster has a magic size. The sp-hybridization plays a crucial role in AgnSnn clusters. For both CO and O2 adsorption, the effect of the Ag4Sn4 cluster is better than that of the Ag8 cluster. The addition of an equal proportion of Sn atoms enhanced the catalysis compared to the Ag8 cluster with the same number of atoms. Our results suggest that the addition of Sn atoms can be an efficient and attractive way of tuning the adsorption ability and reactivity of silver clusters and can provide constructive input for the design of efficient nanocatalysts.

Valorization of Citrus Reticulata Peels for Flavonoids and Antioxidant Enhancement by Solid-State Fermentation Using Aspergillus niger CGMCC 3.6189

The bioactive components and bioactivities of citrus peel can be enhanced with microbial fermentation. Accordingly, this study investigated the ability of Aspergillus niger CGMCC3.6189 to accumulate flavonoids in Citrus reticulata peel powder (CRPP) by solid-state fermentation (SSF). Under the optimal SSF conditions including 80% moisture, 30 °C, pH 4.0, 4 × 107 spores/g d.w. CRPP, and 192 h, the total phenolic content (TPC), total flavonoid content (TFC), and 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) scavenging activities of fermented CRPP significantly increased by 70.0, 26.8, 64.9, and 71.6%, respectively. HPLC analysis showed that after fermentation, the contents of hesperidin, nobiletin, and tangeretin were significantly increased from 19.36, 6.31, and 2.91 mg/g to 28.23, 7.78, and 3.49 mg/g, respectively, while the contents of ferulic acid and narirutin were decreased under the optimal fermentation conditions. Fermentation time is one of the most important factors that affect the accumulation of flavonoids and antioxidant activity; however, extended fermentation time increased the darkness of CRPP color. Therefore, our study provides a feasible and effective SSF method to increase the bioactive components and the antioxidant activity of CRPP that may be used in food, nutraceutical, and medicinal industries.

Adsorption and dissociation of COCl2 on the rutile TiO2(110) surfaces: a systematic first-principles study.

The adsorption and dissociation of phosgene (COCl2) molecules on three kinds of rutile TiO2(110) surfaces (stoichiometric: TiO2-Sto; oxygen defective: TiO2-Ov; and substoichiometric: TiO1.875) were investigated based on density functional theory calculations. The nature of interactions between the COCl2 molecule and rutile TiO2(110) surfaces with different degrees of reduction was researched by the analysis of geometries, electron density difference, adsorption energies and density of states (DOS). Computational results show that COCl2 indicates instability and will dissociate directly without the presence of transition states on a substoichiometric TiO1.875(110) surface. The adsorption and dissociation behavior of COCl2 on the rutile surface is not only helpful in providing theoretical support for the clean and efficient degradation of COCl2, but also helpful in elucidating the role of COCl2 as an intermediate product in the carbochlorination of titanium ore.

MiR-26b-5p inhibits cell proliferation and EMT by targeting MYCBP in triple-negative breast cancer.

BACKGROUND: The study was designed to elucidate the association and functional roles of miR-26b-5p and c-MYC binding protein (MYCBP) in triple-negative breast cancer (TNBC). METHOD: Luciferase reporter assay was used to confirm the relationship between miR-26b-5p and MYCBP in TNBC cells. The expression levels of miR-26b-5p and MYCBP in tissue specimens and cell lines were determined using reverse transcription-quantitative PCR. Cell proliferation, migration and invasion were assessed using CCK-8 assay, colony formation and transwell assay. RESULTS: We first observed that miR-26b-5p directly targets the 3'-UTR of MYCBP to inhibit MYCBP expression in MDA-MB-468 and BT-549 cells. The expression of miR-26b-5p was inversely correlated with MYCBP expression in TNBC tissues. We further demonstrated that MYCBP knockdown suppressed the proliferation, migration and invasion of TNBC cells. Furthermore, MYCBP overexpression counteracted the suppressive effect of miR-26b-5p on TNBC cell behaviors. Western blot analysis demonstrated that the E-cadherin protein level was increased, while protein levels of N-cadherin and vimentin were decreased in cells transfected with miR-26b-5p, which were all reversed by ectopic expression of MYCBP. CONCLUSIONS: In summary, our findings revealed the tumor suppressive role of miR-26b-5p in regulating TNBC cell proliferation and mobility, possibly by targeting MYCBP.

Indicators and prediction models for the severity of Covid-19.

OBJECTIVES: Coronavirus disease 2019 (Covid-19) is outbreaking globally. We aimed to analyse the clinical characteristics, cardiac injury, electrocardiogram and computed tomography (CT) features of patients confirmed Covid-19 and explored the prediction models for the severity of Covid-19. METHODS: A retrospective and single-centre study enrolled 98 laboratory-confirmed Covid-19 patients. Clinical data, electrocardiogram and CT features were collected and analysed using Statistical Package for the Social Sciences software. RESULTS: There were 46 males and 52 females, with a median age of 44 years, categorised into three groups, including mild, moderate and severe/critical Covid-19. The rate of abnormal electrocardiograms in severe/critical group (79%) was significantly higher than that in the mild group (17%) (P = .027), which (r = 0.392, P = .005) positively related to the severity of Covid-19 (OR: 5.71, 95% CI: 0.45-3.04, P = .008). Age older than 60 years old, comorbidities, whether had symptoms on admission, fatigue, CT features, laboratory test results such as platelet count, lymphocyte cell count, eosinophil cell count, CD3+ cell count, CD4+ cell count, CD8+ cell count, the ratio of albumin/globulin decreased and D-dimer, C-reactive protein (CRP), B-type natriuretic peptide (BNP), cardiac troponin I (cTnI) elevated were the risk factors for the increased severity of Covid-19. The logistic model, adjusted by age, lobular involvement score and lymphocyte cell count, could be applied for assessing the severity of Covid-19 (AUC, 0.903; Sensitivity, 90.9%; Specificity, 78.1%). CONCLUSIONS: Age >60 years old, chronic comorbidities, lymphocytopoenia and lobular involvement score were associated with the Covid-19 severity. The inflammation induced by Covid-19 caused myocardial injury with elevated BNP and cTnI level and abnormal electrocardiograms.

Effects of 5-Aza-2'-deoxycytidine on hormone secretion and epigenetic regulation in sika deer ovarian granulosa cells.

5-Aza-2'-deoxycytidine (5-Aza-dC), an inhibitor of DNA methyltransferases, is an effective treatment for various cancers and has improved the development rate of cloned embryos. Previous studies have reported the effect of 5-Aza-dC on fibroblasts; however, the mechanism whereby 5-Aza-dC affects sika deer granulosa cells and hormone secretion is presently unknown. Here, we showed that the cell cycle after treatment with different doses of 5-Aza-dC was significantly altered. The number of cells in the S phase was significantly increased in response to a concentration of 0.1 µM 5-Aza-dC. The rate of apoptosis was increased when cells were treated with 0.1 µM and 5 µM 5-Aza-dC. We showed that the protein level of H3K9me2 was significantly decreased in response to 5-Aza-dC. The activity levels of DNA methyltransferase were reduced by a moderate dose of 5-Aza-dC. Furthermore, the secretion of E2 and P4 was influenced by different doses of 5-Aza-dC. Our study suggested that 5-Aza-dC affected hormone secretion in sika deer granulosa cells through cell development and epigenetic regulation. The findings of this study lay the foundation for further epigenetic studies in sika deer.

Effects of GluN2A and GluN2B gain-of-function epilepsy mutations on synaptic currents mediated by diheteromeric and triheteromeric NMDA receptors.

Mutations in synaptic NMDA receptors (NMDARs) are associated with epilepsy and neurodevelopmental disorders. The effects of several such mutations have been investigated in recombinantly-expressed NMDARs under conditions of steady-state activation. Such experiments provide only limited insight into how mutations affect NMDAR-mediated excitatory synaptic currents (EPSCs). The present study aimed to characterize the effects of the GluN2AN615K, GluN2BN615I and GluN2BV618G gain-of-function mutations on EPSCs mediated by diheteromeric GluN1/2A and GluN1/2B receptors and triheteromeric GluN1/2A/2B receptors, as these are the most abundant synaptic NMDARs in vivo. Subunit composition was controlled by studying 'artificial' synapses formed between cultured neurons (which provide presynaptic terminals) and HEK293 cells that express the NMDAR subunits of interest plus the synapse-promoting molecule, neuroligin-1B. When incorporated into diheteromeric receptors, all three mutations ablated voltage-dependent Mg2+ block of EPSCs, as previously shown. In addition, we were surprised to find that increasing external Mg2+ from 0 to 1 mM strongly enhanced the magnitude of EPSCs mediated by mutant diheteromers. In contrast, triheteromeric receptors exhibited normal voltage-dependent Mg2+ block. The GluN2AN615K mutation also slowed the decay of GluN1/2A/2B- but not GluN1/2A-mediated EPSCs. The GluN2BN615I mutation enhanced the magnitude of both GluN1/2B- and GluN1/2A/2B-mediated EPSCs. The GluN2BV618G mutation enhanced the magnitude of both GluN1/2B- and GluN1/2A/2B-mediated EPSCs, although these effects were partly compensated by a faster EPSC decay rate. The mutations also diminished the potency of the anti-epileptic pore-blocker, memantine, thus explaining the lack of memantine efficacy in patients with GluN2BN615I or GluN2BV618G mutations. Given these effects, the three mutations would be expected to enhance the cation influx rate and thereby contribute to epilepsy phenotypes.

A review on coffee leaves: Phytochemicals, bioactivities and applications.

Coffee leaves have a long history for use as ethnomedicine and tea beverage by locals from countries where coffee plants grow. Recently, attentions have been paid to their health benefits to human beings because of abundant bioactive components in coffee leaves. However, the researches related to the bioactivities, applications, and the impacts of processing methods on the phytochemical composition and activities of coffee leaves are scarce. The reviews specific to coffee leaves in these aspects are rare too. Due to the growing interests to coffee leaves, in this review, the chemical compositions in coffee leaves and the influence of environmental conditions and processing methods on them were summarized. Furthermore, various applications of coffee leaves, including ethnomedicine, coffee leaf tea, therapeutic agent, packaging material, tobacco substitute, organic fungicide, personal hygienic products, and animal feed et al. were presented. The future prospects of coffee leaves are also discussed. In conclusion, coffee leaf is a very promising resource in the areas of food and industry, especially, in the beverage industry. The researches in understanding impacts of the processing methods on the phytochemicals, enzymes, bioactivities, and flavor of coffee leaves are highly needed.

Identification of the JY-1 in sika deer and its effects on granulosa cells cultured in vitro.

The oocyte-specific protein JY-1 was reported as an important regulator of both function of ovarian granulosa cells and early embryogenesis in cattle. Here, we found that the transcripts of JY-1 were also present in sika deer granulosa cells (GCs) through in situ hybridization and qRT-PCR. The complete sika deer JY-1 coding sequence was identified, which had three exons separated by two introns. It was detected that JY-1 knockdown caused apoptosis and abnormal cell cycle progression in GCs of sika deer cultured in vitro. Taken together, these data suggest that JY-1 is involved in the regulation of proliferation in sika deer ovarian GCs.