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A fine global future land use/land cover (LULC) is critical for demonstrating the geographic heterogeneity of earth system dynamics and human-earth interaction. In this study, we produced a 1 km global future LULC dataset that takes into account future climate and socio-economic changes as well as the impact of simulated results of the former year on temporally adjacent periods. By incorporating the variations in climatic and socio-economic factors, we differentiated LULC suitability probabilities for historical and future periods across representative SSP-RCP scenarios. Then, by using an improved cellular automata model-PLUS to simulate the patch-level changes of various land classes, we iteratively downscaled water-basin-level LULC demands in various future scenarios to a spatial resolution of 1 km. Our dataset achieves a high degree of simulation accuracy (Kappa = 0.94, OA = 0.97, FoM = 0.10) and precisely captures the spatial-temporal heterogeneity of global LULC changes under the combined effects of climate change and socio-economic development. This robust and fine-scale LULC dataset provides valuable spatially-explicit information essential for earth system modeling and intricate dynamics between anthropogenic activities and the environment.

Many proteins must translocate through the protein-conducting Sec61 channel in the eukaryotic endoplasmic reticulum membrane or the SecY channel in the prokaryotic plasma membrane 1 , 2 . Proteins with highly hydrophobic signal sequences are first recognized by the signal recognition particle (SRP) 3 , 4 and then moved co-translationally through the Sec61 or SecY channel by the associated translating ribosome. Substrates with less hydrophobic signal sequences bypass the SRP and are moved through the channel post-translationally 5 , 6 . In eukaryotic cells, post-translational translocation is mediated by the association of the Sec61 channel with another membrane protein complex, the Sec62–Sec63 complex 7 – 9 , and substrates are moved through the channel by the luminal BiP ATPase 9 . How the Sec62–Sec63 complex activates the Sec61 channel for post-translational translocation is not known. Here we report the electron cryo-microscopy structure of the Sec complex from Saccharomyces cerevisiae , consisting of the Sec61 channel and the Sec62, Sec63, Sec71 and Sec72 proteins. Sec63 causes wide opening of the lateral gate of the Sec61 channel, priming it for the passage of low-hydrophobicity signal sequences into the lipid phase, without displacing the channel’s plug domain. Lateral channel opening is triggered by Sec63 interacting both with cytosolic loops in the C-terminal half of Sec61 and transmembrane segments in the N-terminal half of the Sec61 channel. The cytosolic Brl domain of Sec63 blocks ribosome binding to the channel and recruits Sec71 and Sec72, positioning them for the capture of polypeptides associated with cytosolic Hsp70 10 . Our structure shows how the Sec61 channel is activated for post-translational protein translocation. The cryo-EM structure of the post-translational protein translocation machinery of the endoplasmic reticulum membrane shows that Sec63 opens the channel, enabling insertion of low-hydrophobicity signal sequences into the lipid phase.

The 2023 work report of the Chinese government underscores a pivotal transition towards a “dual-control” policy, prioritizing the management of carbon emissions. This study provides an in-depth analysis of the interplay between the digital economy, technological progress, and their impact on the total volume and intensity of carbon emissions across 30 Chinese provinces from 2013 to 2021. Our findings reveal that while the expansion of the digital economy and technological progress contribute to an increase in the total carbon emissions, they also markedly decrease carbon intensity, paving the way for sustainability. Additionally, the research uncovers the positive externalities of the digital economy on carbon emission intensity and the spillover effects of technological progress on both emissions and intensity. The integration of the digital economy in industrial restructuring and the uptake of green technologies are identified as instrumental in mitigating carbon emissions. These insights underscore the potential of policy strategies that leverage the digital economy and technological innovation to meet the “dual-control” policy objectives and foster sustainable development.

Lysine lactylation (Kla) links metabolism and gene regulation and plays a key role in multiple biological processes. However, the regulatory mechanism and functional consequence of Kla remain to be explored. Here, we report that HBO1 functions as a lysine lactyltransferase to regulate transcription. We show that HBO1 catalyzes the addition of Kla in vitro and intracellularly, and E508 is a key site for the lactyltransferase activity of HBO1. Quantitative proteomic analysis further reveals 95 endogenous Kla sites targeted by HBO1, with the majority located on histones. Using site-specific antibodies, we find that HBO1 may preferentially catalyze histone H3K9la and scaffold proteins including JADE1 and BRPF2 can promote the enzymatic activity for histone Kla. Notably, CUT&Tag assays demonstrate that HBO1 is required for histone H3K9la on transcription start sites (TSSs). Besides, the regulated Kla can promote key signaling pathways and tumorigenesis, which is further supported by evaluating the malignant behaviors of HBO1- knockout (KO) tumor cells, as well as the level of histone H3K9la in clinical tissues. Our study reveals HBO1 serves as a lactyltransferase to mediate a histone Kla-dependent gene transcription. The regulatory mechanism and functional consequence of lysine lactylation remain to be explored. Here, the authors identify HBO1 as a lysine lactyltransferase and suggest a potential role of HBO1 in tumorigenesis through H3K9la-mediated transcription regulation.

Amides are versatile synthetic building blocks and their selective transformations into highly valuable functionalities are much desirable in the chemical world. However, the diverse structure and generally high stability of amides make their selective transformations challenging. Here we disclose a chemodivergent transformation of primary, secondary and tertiary amides by using 1,1-diborylalkanes as pro-nucleophiles. In general, selective B-O elimination occurs for primary, secondary amides and tertiary lactams to generate enamine intermediate, while tertiary amides undergo B-N elimination to generate enolate intermediate. Various in situ electrophilic trapping of those intermediates allows the chemoselective synthesis of α-functionalized ketones, β-aminoketones, enamides, β-ketoamides, γ-aminoketones, and cyclic amines from primary, secondary, tertiary amides and lactams. The key for these transformations is the enolization effect after the addition of α-boryl carbanion to amides. Amides are versatile synthetic building blocks, however the general stability of the amide bond makes its selective transformation challenging. Here, the authors report a chemodivergent transformation of primary, secondary and tertiary amides by using 1,1-diborylalkanes as pro-nucleophiles.

N6-methyladenosine (m6A) stands as the most prevalent modified form of RNA in eukaryotes, pivotal in various biological processes such as regulating RNA stability, translation, and transcription. All members within the YT521-B homology (YTH) gene family are categorized as m6A reading proteins, capable of identifying and binding m6A modifications on RNA, thereby regulating RNA metabolism and functioning across diverse physiological processes. YTH domain-containing 2 (YTHDC2), identified as the latest member of the YTH family, has only recently started to emerge for its biological function. Numerous studies have underscored the significance of YTHDC2 in human physiology, highlighting its involvement in both tumor progression and non-tumor diseases. Consequently, this review aims to further elucidate the pathological mechanisms of YTHDC2 by summarizing its functions and roles in tumors and other diseases, with a particular focus on its downstream molecular targets and signaling pathways.

Robot technology has important application value in coal mines, non-coal mines, and other fields. However, the existing coal gangue multi-task allocation methods cannot be used for the coal foreign object with multi kinds, complex features, and spatiotemporal randomness, and it is difficult to solve comprehensively improve coal quality, human–machine safety and environmental pollution. Firstly, this paper constructs a multi-task allocation model of coal foreign object sorting robot (CFoSR) based on optimal capacity and benefit. The matching function, optimal capacity function and benefit function were used to calculate the environmental state matrix, and the state transfer function was designed to update the environmental state, which described the multi-task allocation problem of coal foreign object sorting. Then, a multi-evaluation index fitness function was designed that comprehensively considered the total mass of gangue sorting and the total number of sundry sorting. According to the scheduling rules such as first-in-first-out (FIFO), benefit first (BF) and shortest process time (SPT), a combined rule strategy based on genetic algorithm (GACRS) is proposed. Finally, the CFoSR simulation environment was built. The action mechanism of scheduling rules, heterogeneous manipulators, belt speed and coal flow upper limit on the multi-task allocation results of CFoSR is deeply analyzed. The simulation results show that the optimal fitness value of GACRS is 24.73% higher than that of adaptive weights based on greedy algorithm(GAW). The comparison results based on CFoSR experimental platform show that the optimal fitness value of GACRS is 14.02% higher than that of GAW. This paper provides a multi-task allocation model and its solution method for intelligent coal foreign object sorting.

Lung cancer is the second cancer and the leading cause of tumor-related mortality worldwide. Angiogenesis is a crucial hallmark of cancer development and a promising target in lung cancer. However, the anti-angiogenic drugs currently used in the clinic do not achieve long-term efficacy and are accompanied by severe adverse reactions. Therefore, the development of novel anti-angiogenic therapeutic approaches for lung cancer is urgently needed. Non-coding RNAs (ncRNAs) participate in multiple biological processes in cancers, including tumor angiogenesis. Many studies have demonstrated that ncRNAs play crucial roles in tumor angiogenesis. This review discusses the regulatory functions of different ncRNAs in lung cancer angiogenesis, focusing on the downstream targets and signaling pathways regulated by these ncRNAs. Additionally, given the recent trend towards utilizing ncRNAs as cancer therapeutics, we also discuss the tremendous potential applications of ncRNAs as biomarkers or novel anti-angiogenic tools in lung cancer.

Dynamic spatial patterns of signaling factors or macromolecular assemblies in the form of oscillations or traveling waves have emerged as important themes in cell physiology. Feedback mechanisms underlying these processes and their modulation by signaling events and reciprocal cross-talks remain poorly understood. Here we show that antigen stimulation of mast cells triggers cyclic changes in the concentration of actin regulatory proteins and actin in the cell cortex that can be manifested in either spatial pattern. Recruitment of FBP17 and active Cdc42 at the plasma membrane, leading to actin polymerization, are involved in both events, whereas calcium oscillations, which correlate with global fluctuations of plasma membrane PI(4,5)P ₂, are tightly linked to standing oscillations and counteract wave propagation. These findings demonstrate the occurrence of a calcium-independent oscillator that controls the collective dynamics of factors linking the actin cytoskeleton to the plasma membrane. Coupling between this oscillator and the one underlying global plasma membrane PI(4,5)P2 and calcium oscillations spatially regulates actin dynamics, revealing an unexpected pattern-rendering mechanism underlying plastic changes occurring in the cortical region of the cell.

Arginine vasopressin (AVP) and oxytocin (OT) are peptide hormones critical for various physiological processes. Vasopressin receptor 1 A (V1aR), a primary AVP target, is promising for central nervous system (CNS) disorders therapies, yet the mechanisms of antagonism and oligomerization remain poorly understood. Here, we present structures of human V1aR in its apo state and in complexes with antagonists: atosiban, balovaptan, and SRX246. Structural analyses reveal a dimeric V1aR assembly, validated by functional assays and imaging in cells. The apo structure shows a flat extracellular loop 2 (ECL2) with unpaired cysteines, undergoing significant conformational changes upon ligand binding. Antagonist-bound structures, combined with mutagenesis and radioligand binding assays, uncover distinct binding modes and key determinants for antagonism and selectivity. These findings provide a comprehensive understanding of V1aR assembly and dynamic regulation, offering valuable insights for structure-guided development of new antagonists targeting dimeric V1aR for CNS disorders. Authors in this study report cryo-EM structures of human V1aR in its apo state and in complexes with antagonists. Structural analyses reveal a dimeric assembly, flat ECL2 with unpaired cysteines in apo state, and uncover distinct binding modes and key determinants for antagonism and selectivity.