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The combination of genome editing and primordial germ cell (PGC) transplantation has enormous significance in the study of developmental biology and genetic breeding, despite its low efficiency due to limited number of donor PGCs. Here, we employ a combination of germplasm factors to convert blastoderm cells into induced PGCs (iPGCs) in zebrafish and obtain functional gametes either through iPGC transplantation or via the single blastomere overexpression of germplasm factors. Zebrafish-derived germplasm factors convert blastula cells of Gobiocypris rarus into iPGCs, and Gobiocypris rarus spermatozoa can be produced by iPGC-transplanted zebrafish. Moreover, the combination of genome knock-in and iPGC transplantation perfectly resolves the contradiction between high knock-in efficiency and early lethality during embryonic stages and greatly improves the efficiency of genome knock-in. Together, we present an efficient method for generating PGCs in a teleost, a technique that will have a strong impact in basic research and aquaculture. Primordial germ cell (PGC) transplantation is an important technology for developmental biology and genetic breeding. Here, Wang et al. develop an approach for PGC induction that enhances the efficiency of PGC transplantation in zebrafish.

Maternal β-catenin activity is essential and critical for dorsal induction and its dorsal activation has been thoroughly studied. However, how the maternal β-catenin activity is suppressed in the nondorsal cells remains poorly understood. Nanog is known to play a central role for maintenance of the pluripotency and maternal -zygotic transition (MZT). Here, we reveal a novel role of Nanog as a strong repressor of maternal β-catenin signaling to safeguard the embryo against hyperactivation of maternal β-catenin activity and hyperdorsalization. In zebrafish, knockdown of nanog at different levels led to either posteriorization or dorsalization, mimicking zygotic or maternal activation of Wnt/β-catenin activities, and the maternal zygotic mutant of nanog (MZnanog) showed strong activation of maternal β-catenin activity and hyperdorsalization. Although a constitutive activator-type Nanog (Vp16-Nanog, lacking the N terminal) perfectly rescued the MZT defects of MZnanog, it did not rescue the phenotypes resulting from β-catenin signaling activation. Mechanistically, the N terminal of Nanog directly interacts with T-cell factor (TCF) and interferes with the binding of β-catenin to TCF, thereby attenuating the transcriptional activity of β-catenin. Therefore, our study establishes a novel role for Nanog in repressing maternal β-catenin activity and demonstrates a transcriptional switch between β-catenin/TCF and Nanog/TCF complexes, which safeguards the embryo from global activation of maternal β-catenin activity.

Genome-wide association studies (GWASs) are the most widely used method to identify genetic risk loci associated with orofacial clefts (OFC). However, despite the increasing size of cohort, GWASs are still insufficient to detect all the heritability, suggesting there are more associations under the current stringent statistical threshold. In this study, we obtained an integrated epigenomic dataset based on the chromatin conformation of a human oral epithelial cell line (HIOEC) using RNA-seq, ATAC-seq, H3K27ac ChIP-seq, and DLO Hi-C. Presumably, this epigenomic dataset could reveal the missing functional variants located in the oral epithelial cell active enhancers/promoters along with their risk target genes, despite relatively less-stringent statistical association with OFC. Taken a non-syndromic cleft palate only (NSCPO) GWAS data of the Chinese Han population as an example, 3664 SNPs that cannot reach the strict significance threshold were subjected to this functional identification pipeline. In total, 254 potential risk SNPs residing in active cis-regulatory elements interacting with 1 718 promoters of oral epithelium-expressed genes were screened. Gapped k-mer machine learning based on enhancers interacting with epithelium-expressed genes along with in vivo and in vitro reporter assays were employed as functional validation. Among all the potential SNPs, we chose and confirmed that the risk alleles of rs560789 and rs174570 reduced the epithelial-specific enhancer activity by preventing the binding of transcription factors related to epithelial development. In summary, we established chromatin conformation datasets of human oral epithelial cells and provided a framework for testing and understanding how regulatory variants impart risk for clefts.

The present paper investigates monitoring of fatigue cracks of a metal structure using an eddy current micro sensor. Fatigue cracks tend to occur at bolt-jointed structures on an aircraft. In order to detect the damage quantitatively, a kind of change-prone micro eddy current sensor is designed and fabricated with flexible printed circuit board (FPCB) technology. A forward semi-analytical model is built by extracting a material’s conductivity as the damage feature parameter, and characteristics analysis is conducted based on the model. The research focuses on setting up and utilizing the eddy current fields to analyze interaction of adjoining coils when the damage occurs, and investigating optimization on the working parameters of the sensor. In the experimental section, several common connection structures are applied to explore the sensor’s monitoring ability both in air and in a corrosive environment. The result shows that the optimal working frequency is about 1 MHz. The eddy current micro sensor is capable of monitoring the crack growth with an accuracy of 1 mm, the average error being 4.6 % compared to fracture analysis. The sensor keeps high resolution of damage in aqueous corrosion. Due to the fretting fatigue, wear appears on the polyimide foil, leading to the decreases of the monitoring signal.

Maternal [beta]-catenin activity is essential and critical for dorsal induction and its dorsal activation has been thoroughly studied. However, how the maternal [beta]-catenin activity is suppressed in the nondorsal cells remains poorly understood. Nanog is known to play a central role for maintenance of the pluripotency and maternal -zygotic transition (MZT). Here, we reveal a novel role of Nanog as a strong repressor of maternal [beta]-catenin signaling to safeguard the embryo against hyperactivation of maternal [beta]-catenin activity and hyperdorsalization. In zebrafish, knockdown of nanog at different levels led to either posteriorization or dorsalization, mimicking zygotic or maternal activation of Wnt/[beta]-catenin activities, and the maternal zygotic mutant of nanog (MZnanog) showed strong activation of maternal [beta]-catenin activity and hyperdorsalization. Although a constitutive activator-type Nanog (Vp16-Nanog, lacking the N terminal) perfectly rescued the MZT defects of MZnanog, it did not rescue the phenotypes resulting from [beta]-catenin signaling activation. Mechanistically, the N terminal of Nanog directly interacts with T-cell factor (TCF) and interferes with the binding of [beta]-catenin to TCF, thereby attenuating the transcriptional activity of [beta]-catenin. Therefore, our study establishes a novel role for Nanog in repressing maternal [beta]-catenin activity and demonstrates a transcriptional switch between [beta]-catenin/TCF and Nanog/TCF complexes, which safeguards the embryo from global activation of maternal [beta]-catenin activity.

The cyclic load number of aero-engine blade during its service life is very likely beyond 107, which is regarded as the conventional fatigue limit. Moreover, surface strengthening is very often used in the manufacturing process of blade. The conventional testing method in the VHCF regime cannot exactly reflect the stress state of the blade, including the mechanism of crack initiation. To study the fatigue behavior and effects of laser shock peening, a kind of bending fatigue subcomponent specimen was designed and the laser shock peening model was established. Experiment about TC17 was accomplished by the Ulra-High Cycle bending fatigue system. It is found that the fatigue damage occurs beneath the surface and the S-N curve is continuously rather than multi-step declining in the VHCF regime. Process of surface strengthening has a significant effect on fatigue performance of TC17 titanium alloy.

Many maternal mRNAs are translationally repressed during oocyte maturation and spatio-temporally activated during early embryogenesis, which is critical for oocyte and early embryo development. By analyzing maternal mutants of nanog (Mnanog) in zebrafish, we demonstrated that Nanog tightly controls translation of maternal mRNA during oocyte maturation via transcriptional repression of eukaryotic translation elongation factor 1 alpha 1, like 2 (eef1a1l2). Loss of maternal Nanog led to defects of egg maturation, increased endoplasmic reticulum (ER) stress, and an activated unfold protein response (UPR), which was caused by elevated translational activity. We further demonstrated that Nanog, as a transcriptional repressor, represses the transcription of eefl1a1l2 by directly binding to the eef1a1l2 promoter during oocyte maturation. More importantly, depletion of eef1a1l2 in nanog mutant females effectively rescued the elevated translational activity in oocytes, egg quality defects, and embryonic defects of Mnanog embryos. Thus, our study demonstrates that maternal Nanog regulates oocyte maturation and early embryogenesis though translational control of maternal mRNA via a novel mechanism, in which Nanog acts as a transcriptional repressor to suppress transcription of eef1a1l2.

Maternal β-catenin activity is essential and critical for dorsal induction and its dorsal activation has been thoroughly studied. However, how the maternal β-catenin activity is suppressed in the non-dorsal cells remains poorly understood. Nanog is known to play a central role for maintenance of the pluripotency and maternal-to-zygotic transition. Here we reveal a novel role of Nanog as a strong repressor of maternal Wnt/β-catenin signaling to safeguard the embryo against hyper-activation of maternal β-catenin activity and hyper-dorsalization. Knockdown of nanog at different levels led to either posteriorization or dorsalization, mimicking zygotic or maternal activation of Wnt/β-catenin activities, and the maternal-zygotic mutant of nanog (MZnanog) showed strong activation of maternal β-catenin and hyper-dorsalization. Although a constitutive-activator-type Nanog (Vp16-Nanog, lacking the N-terminal) perfectly rescued the defects of maternal to zygotic transition in MZnanog, it did not rescue the phenotypes resulting from β-catenin activation. Mechanistically, the N-terminal of Nanog directly interacts with TCF and interferes with the binding of β-catenin to TCF, thereby attenuating the transcriptional activity of β-catenin. Therefore, our study establishes a novel role for Nanog in repressing maternal β-catenin activity and demonstrates a transcriptional switch between β-catenin/TCF and Nanog/TCF complexes, which safeguards the embryo from global activation of maternal β-catenin activity.

In this work, we investigate the capacity allocation problem in the energy harvesting wireless sensor networks (WSNs) with interference channels. For the fixed topologies of data and energy, we formulate the optimization problem when the data flow remains constant on all data links and each sensor node harvests energy only once in a time slot. We focus on the optimal data rates, power allocations and energy transfers between sensor nodes in a time slot. Our goal is to minimize the total delay in the network under two scenarios, i.e., no energy transfer and energy transfer. Furthermore, since the optimization problem is non-convex and difficult to solve directly, by considering the network with the relatively high signal-to-interference-plus-noise ratio (SINR), the non-convex optimization problem can be transformed into a convex optimization problem by convex approximation. We attain the properties of the optimal solution by Lagrange duality and solve the convex optimization problem by the CVX solver. The experimental results demonstrate that the total delay of the energy harvesting WSNs with interference channels is more than that in the orthogonal channel; the total network delay increases with the increasing data flow for the fixed energy arrival rate; and the energy transfer can help to decrease the total delay.

The ZrB 2 /A356 composite material was prepared by using chemical in situ reaction technology. The high-temperature friction and wear test of ZrB 2 /A356 aluminum matrix composites was carried out. The friction and wear test temperatures were normal temperatures, 50 °C, 100 °C, 150 °C, 200 °C, 250 °C, and 300 °C. XRD, TEM, SEM, and XPS were used to analyze the microstructure, phase and the formation of surface compounds of the composites under different wear temperatures. The results show that the composite phase is composed of ZrB 2 and ɑ-Al, and there is a small amount of Al-Si eutectic phase; ZrB 2 particles are small, hexagonal nearly elliptical, flocculent and well bonded to the matrix; Combined with the stress-strain curve and tensile fracture morphology analysis, the composite material is a ductile fracture, and the plasticity of the A356 alloy is higher than that of the composite material; The wear properties of composites are susceptible to temperature changes, and the wear rate is small below 200 °C. The wear mechanism is mainly oxidative wear and abrasive wear. When the temperature reaches above 250 °C, the wear rate begins to rise sharply, and a large number of plastic deformation traces and wear debris appear on the surface of the wear spot, and the surface of the wear debris adheres to the protrusions. The primary wear mechanism is adhesive wear. In the stages of oxidative wear, and abrasive wear, although the friction coefficient changes, it is stable. But in the adhesive wear stage, the friction coefficient becomes very unstable and a sharp peak appears. XPS analysis showed that the compounds formed in the wear scar were mainly Al 2 O 3 .