An Asymmetric Galactic Stellar Disk Traced by OB-type Stars from LAMOST DR7

Using 9943 OB-type stars from LAMOST DR7 in the solar neighborhood,we fit the vertical stellar density profile with the model including a single exponential distribution at different positions(R,Φ).The distributions of the scale heights and scale length show that the young disk traced by the OB-type stars is not axisymmetric.The scale length decreases versus the azimuthal angleΦ,i.e.,from.■kpc withΦ=-3°to■kpc withΦ=9°.Meanwhile we find signal of non-symmetry in the distribution of the scale height of the north and south of the disk plane.The scale height in the north side shows signal of flaring of the disk,while that of the south disk stays almost constant around h_(s)=130 pc.The distribution of the displaceeent of the disk plane Z_(0)also shows variance versus the azimuthal angleΦ,which displays significant differences with the warp model constrained by the Cepheid stars.We also test different values for the position of the Sun,and the distance between the Sun and the Galactic center affects the scale heights and the displacement of the disk significantly,but that does not change our conclusion that the disk is not axisymmetric.

Transcriptome Dynamics and Cell Dialogs Between Oocytes and Granulosa Cells in Mouse Follicle Development

The development and maturation of follicles is a sophisticated and multistage process.The dynamic gene expression of oocytes and their surrounding somatic cells and the dialogs between these cells are critical to this process.In this study,we accurately classified the oocyte and follicle development into nine stages and profiled the gene expression of mouse oocytes and their surrounding granulosa cells and cumulus cells.The clustering of the transcriptomes showed the trajectories of two distinct development courses of oocytes and their surrounding somatic cells.Gene expression changes precipitously increased at Type 4 stage and drastically dropped afterward within both oocytes and granulosa cells.Moreover,the number of differentially expressed genes between oocytes and granulosa cells dramatically increased at Type 4 stage,most of which persistently passed on to the later stages.Strikingly,cell communications within and between oocytes and granulosa cells became active from Type 4 stage onward.Cell dialogs connected oocytes and granulosa cells in both unidirectional and bidirectional manners.TGFB2/3,TGFBR2/3,INHBA/B,and ACVR1/1B/2B of TGF-βsignaling pathway functioned in the follicle development.NOTCH signaling pathway regulated the development of granulosa cells.Additionally,many maternally DNA methylation-or H3K27me3-imprinted genes remained active in granulosa cells but silent in oocytes during oogenesis.Collectively,Type 4 stage is the key turning point when significant transcription changes diverge the fate of oocytes and granulosa cells,and the cell dialogs become active to assure follicle development.These findings shed new insights on the transcriptome dynamics and cell dialogs facilitating the development and maturation of oocytes and follicles.

Nuclear m^(6)A reader YTHDC1 regulates the scaffold function of LINE1 RNA in mouse ESCs and early embryos

N^(6)-methyladenosine(m^(6)A)on chromosome-associated regulatory RNAs(carRNAs),including repeat RNAs,plays important roles in tuning the chromatin state and transcription,but the intrinsic mechanism remains unclear.Here,we report that YTHDC1 plays indispensable roles in the self-renewal and differentiation potency of mouse embryonic stem cells(ESCs),which highly depends on the m^(6)A-binding ability.Ythdcl is required for sufficient rRNA synthesis and repression of the 2-cell(2C)transcriptional program in ESCs,which recapitulates the transcriptome regulation by the LINE1 scaffold.Detailed analyses revealed that YTHDC1 recognizes m^(6)A on LINE1 RNAs in the nucleus and regulates the formation of the LINE1-NCL partnership and the chromatin recruitment of KAP1.Moreover,the establishment of H3K9me3 on 2C-related retrotrans-posons is interrupted in Ythdcl-depleted ESCs and inner cell mass(ICM)cells,which consequently increases the transcriptional activities.Our study reveals a role of m^(6)A in regulating the RNA scaffold,providing a new model for the RNA-chromatin cross-talk.

METTL14 is a chromatin regulator independent of its RNA N^(6)-methyladenosine methyltransferase activity

METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m^(6)A methyltransferase complex(MTC)that installs m^(6)A.Surprisingly,depletion of METTL3 or METTL14 displayed distinct effects on stemness maintenance of mouse embryonic stem cell(mESC).While comparable global hypo-methylation in RNA m^(6)A was observed in Mettl3 or Mettl14 knockout mESCs,respectively.Mettl14 knockout led to a globally decreased nascent RNA synthesis,whereas Mettl3 depletion resulted in transcription upregulation,suggesting that METTL14 might possess an mA-independent role in gene regulation.We found that METTL14 colocalizes with the repressive H3K27me3 modification.Mechanistically,METTL14,but not METTL3,binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3.Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression.The effects of METTL14 on regulation of H3K27me3 is essential for the transition from self-renewal to differentiation of mESCs.This work reveals a regulatory mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m^(6)A,and critically impacts transcriptional regulation,stemness maintenance,and differentiation ofmESCs.

Esrrb plays important roles in maintaining self-renewal of trophoblast stem cells (TSCs) and reprogramming somatic cells to induced TSCs

Trophoblast stem cells (TSCs), which can be derived from the trophoectoderm of a blastocyst, have the ability to sustain self-renewal and differentiate into various placental trophoblast cell types. Meanwhile, essential insights into the molecular mechanisms controlling the placental development can be gained by using TSCs as the cell model. Esrrb is a transcription factor that has been shown to play pivotal roles in both embryonic stem cell (ESC) and TSC, but the precise mechanism whereby Esrrb regulates TSC-specific transcriptome during differentiation and reprogramming is still largely unknown. In the present study, we elucidate the function of Esrrb in self-renewal and differentiation of TSCs, as well as during the induced TSC (iTSC) reprogramming. We demonstrate that the precise level of Esrrb is critical for stem state maintenance and further trophoblast differentiation of TSCs, as ectopically expressed Esrrb can partially block the rapid differentiation of TSCs in the absence of fibroblast growth factor 4. However, Esrrb depletion results in downregulation of certain key TSC-specific transcription factors, consequently causing a rapid differentiation of TSCs and these Esrrb-deficient TSCs lose the ability of hemorrhagic lesion formation in vivo. This function of Esrrb is exerted by directly binding and activating a core set of TSC-specific target genes including Cdx2, Eomes, Sox2, Fgfr4, and Bmp4. Furthermore, we show that Esrrb overexpression can facilitate the MEF-to-iTSC conversion. Moreover, Esrrb can substitute for Eomes to generate GEsTM-iTSCs. Thus, our findings provide a better understanding of the molecular mechanism of Esrrb in maintaining TSC self-renewal and during iTSC reprogramming.

INDEEDopt:a deep learning-based ReaxFF parameterization framework

Empirical interatomic potentials require optimization of force field parameters to tune interatomic interactions to mimic ones obtained by quantum chemistry-based methods.The optimization of the parameters is complex and requires the development of new techniques.Here,we propose an INitial-DEsign Enhanced Deep learning-based OPTimization(INDEEDopt)framework to accelerate and improve the quality of the ReaxFF parameterization.The procedure starts with a Latin Hypercube Design(LHD)algorithm that is used to explore the parameter landscape extensively.The LHD passes the information about explored regions to a deep learning model,which finds the minimum discrepancy regions and eliminates unfeasible regions,and constructs a more comprehensive understanding of physically meaningful parameter space.We demonstrate the procedure here for the parameterization of a nickel–chromium binary force field and a tungsten–sulfide–carbon–oxygen–hydrogen quinary force field.We show that INDEEDopt produces improved accuracies in shorter development time compared to the conventional optimization method.

Er-Y-Cr-Si化合物在极低温区的巨低场磁热效应

高性能低温低场磁热材料在气体液化等领域具有重要的应用前景.本团队通过真空电弧熔炼的方式成功合成了一系列多晶Er_(1-x)Y_(x)Cr_(2)Si_(2)(0≤x≤0.8)样品,这些材料表现出巨大的低场磁热效应.其中Cr含量为0.1的样品显示出最好的低场磁热性能以及接近2 K的合适的工作温区.更重要的是,在0-1 T的磁场变化下,该样品的最大磁熵变峰值以及最大绝热温变峰值分别高达19.2 J kg^(-1)K^(-1)和4.3 K.其磁熵变峰值为目前已报道的20 K以下温区合金类磁热材料的最大值.通过Arrott曲线,平均场理论以及约化磁熵变曲线等手段,证明了磁相变特征为二级相变.物理机理分析表明,10%的Y替代导致高达15.9%的磁熵变峰值增强的原因在于替代样品所具有的大饱和磁化强度以及小饱和磁场.

ABE-induced PDGFD start codon silencing unveils new insights into the genetic architecture of sheep fat tails

Sheep is an important livestock species raised globally to produce meat,milk,wool,and other by-products.During the Neolithic Revolution,sheep were domesticated in the Fertile Crescent of Southwest Asia around 10,000 years ago(Chessa et al.,2009).

Correction to:Nuclear m6A reader YTHDC1 regulates the scaffold function of LINE1 RNA in mouse ESCs and early embryos

CORRECTION TO:PROTEIN CELL(2021)HTTPS://DOI.ORG/10.1007/S13238-021-00837-8 In the original publication of the article figure 1 is incorrectly published.The correct Figure 1 is provided in this correction.OPEN ACCESS This article is licensed under a Creative Commons Attribution 4.0 International License,which permits use,sharing,adaptation,distribution and reproduction in any medium or format,as long as you give appropriate credit to the original author(s)and the source,provide a link to the Creative Commons licence,and indicate if changes were made.The images or other third party material in this article are included in the article's Creative Commons licence,unless indicated otherwise in a credit line to the material.If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use,you will need to obtain permission directly from the copyright holder.To view a copy of this licence,visit https://creativecommons.org/licenses/by/4.0/.