Science China Life Sciences最新文献

Diurnal floret opening and closure (DFOC) is essential for rice reproductive development and hybrid breeding, yet transcriptional dynamics and underlying regulatory networks remain poorly characterized. Here, we conducted high-temporal-resolution transcriptomic analyses of lodicules to dissect DFOC regulatory networks in two japonica rice cultivars. Analysis of differentially expressed genes (DEGs) uncovered core genes shared by both cultivars, primarily associated with jasmonic acid (JA) signaling and cell wall remodeling. By integrating DNA affinity purification sequencing (DAP-seq), we constructed core regulatory networks mediated by the basic helix-loop-helix transcription factor (TF) OsMYC2, governing DFOC in rice. We identified xyloglucan endotransglycosylase-related gene 1 (OsXTR1), which encodes a cell-wall loosening enzyme, as a key gene activated by OsMYC2 during DFOC. Disruption of OsXTR1 resulted in florets failing to close after opening, demonstrating its essential role in linking cell wall dynamics to hormonal regulation. Similarly, we identified a JA biosynthesis gene, allene oxide cyclase (OsAOC), which is implicated in DFOC through an OsMYC2-mediated positive-feedback loop. Additionally, we developed the RiceDFOC database ( http://zhoulab.zju.edu.cn/FT/index.html ), providing interactive access to spatiotemporal transcriptomes, co-expression networks, and phenomics data. Collectively, our study unveils a hierarchical OsMYC2-centric network that coordinates JA signaling and structural remodeling during DFOC, providing mechanistic insights and resources for optimizing rice breeding.

Light, as an important environmental factor, has a crucial influence on the life activities of fungi. Botrytis cinerea is a typical light-responsive filamentous fungus capable of coordinating its growth and development with ambient light signals. Here, we find that Bcmads1, a key transcription factor in the light signaling pathway, can regulate the accumulation of many metabolites in a light-dependent manner, and demonstrate that N-vanillylnonanamide plays an important role in Bcmads1-regulated photomorphogenesis. Then, we confirm that Bcmads1 can directly regulate the expression of BcAMT1, which further affects the photomorphogenesis of B. cinerea by catalyzing the reaction from vanillin to vanillylamine in the N-vanillylnonanamide synthesis pathway. We find a new pathway of light signal transduction in B. cinerea and elucidate the new mechanism of Bcmads1 regulating N-vanillylnonanamide synthesis involved in the photomorphogenesis of B. cinerea.

Chronic hepatitis B is perpetuated by the presence of covalently closed circular DNA (cccDNA) from the hepatitis B virus (HBV) in the liver's hepatocytes. Despite these efforts, the exact mechanisms by which the chromatin structure of cccDNA enables viral persistence remain unclear. This study investigates the vital role of mammalian SWI/SNF chromatin remodeling complexes in regulating the transcriptional activity of cccDNA. Our research, using pharmacological inhibitors and genetic techniques, identifies BRG1 (SMARCA4), the central ATPase of the mSWI/SNF complexes, and BRD9, a non-canonical BAF (ncBAF)-specific subunit, as crucial host factors for HBV replication. The overexpression of SMARCA4 enhances viral propagation, whereas its targeted degradation using PROTAC AU15330 or siRNA significantly reduces cccDNA-driven transcription, viral transcripts, and protein levels. Chromatin accessibility assays demonstrate that the depletion of BRG1 (SMARCA4) compacts the chromatin at critical cccDNA regulatory regions. Mechanistically, the HBV X protein (HBx) interacts with BAF155 and collaborates with transcription factor YY1 to promote the SWI/SNF complex binding to viral chromatin. Interestingly, inhibiting BRD9, an ncBAF-specific acetyl-lysine reader, similarly disrupts cccDNA transcription, indicating a coordinated function of canonical and non-canonical SWI/SNF complexes via acetylation-dependent chromatin remodeling. These insights highlight SWI/SNF complexes as key regulators of viral persistence and suggest targeting these complexes as a potential therapeutic strategy for eradicating cccDNA reservoirs, potentially leading to a functional cure for chronic HBV infection.

Plant growth-promoting rhizobacteria (PGPR) are beneficial microorganisms residing in the rhizosphere that enhance plant growth and health. While fundamental research on established PGPR strains has focused on their biological functions and interactions with plants, in-depth investigations of root colonization mechanisms and microbial interactions within the rhizosphere remain limited. This review presents Bacillus velezensis SQR9 as a model PGPR strain, affirming its inclusion of conventional plant-beneficial mechanisms, including antimicrobial metabolite production, induced systemic resistance, resource competition, phytohormone production, along with novel mechanisms unique to SQR9, such as root development enhancement, nitrogen uptake promotion, and abiotic stress tolerance. The complex processes and molecular mechanisms of root colonization-including spore germination, chemotaxis, adhesion, immune evasion, and biofilm formation-are summarized. Furthermore, the influence of SQR9 on plant microbiomes and its interactions with other soil microorganisms are examined, paving the way for leveraging beneficial microbial interactions to enhance the functionality of PGPRs. We also assess the biotechnological potential of SQR9, supported by multiple patents and successful commercial applications in biofertilizer production. By elucidating the specific roles and benefits of B. velezensis SQR9, this review serves as a practical guide for developing innovative PGPR-based solutions aimed at enhancing crop yields and promoting sustainable agricultural practices.

Controllable targeted protein degradation (controllable TPD) technologies, exemplified by proteolysis-targeting chimeras (PROTACs), have emerged as transformative tools in drug discovery and molecular biology research. With the endogenous cellular degradation machinery, controllable TPD platforms allow for the precise targeting and regulated elimination of specific proteins within cells. Recent advances have expanded the spectrum of controllable degradation strategies, including photosensitive degrons, opto-PROTACs, auxin-inducible degron (AID) systems, small molecule-assisted shut-off (SMASh) techniques, and engineered E3 ubiquitin ligases such as ΔTRIM21 with enhanced targeted protein degradation efficiency (ΔTRIM-TPD). These emerging methodologies provide unprecedented control over protein stability, facilitating targeted therapeutic interventions for diseases such as cancer and infectious diseases, and significantly advancing fundamental biological research. This review systematically summarizes recent breakthroughs in controllable TPD strategies, elucidates their distinct molecular mechanisms, and highlights their promising therapeutic applications. The rapidly evolving field of controllable TPD represents a powerful and adaptable technological frontier, opening new avenues in precision medicine and providing versatile tools for the future of biomedical research.

Mechanical signaling plays a crucial yet poorly understood role in human neural tube morphogenesis. In this study, we elucidate how the Hippo pathway mechanosensor YAP converts apical tension into transcriptional programs to guide this process. Using human cortical organoids, we demonstrated that YAP accumulates and translocates to the nucleus within high-tension apical domains of neural rosettes. YAP depletion disrupted apicobasal epithelial polarity, manifested as disorganized cytoskeleton, compromised tight junctions, and impaired ciliogenesis, which ultimately resulted in defective rosette morphogenesis. Mechanistically, the YAP-TEAD4 complex transcriptionally activated LEF1, a central regulator of Wnt signaling. LEF1 deficiency phenocopied YAP loss, whereas its overexpression partially rescued rosette defects. Our findings establish the YAP-LEF1 axis as a critical integrator of mechanical and morphogenetic signals in neural tube development, thereby highlighting its potential as a therapeutic target for neural tube defects such as anencephaly.

The growing wealth of single-cell omics datasets presents unprecedented opportunities to uncover new insights into temporal gene dynamics during development. However, this relies on accessible, diverse time-series data and robust in-silico analysis methods-resources that are underutilized in current databases. Herein, we present TEDD 2.0 ( https://tedd.obg.cuhk.edu.hk/ ), an enhanced version of our Temporal Expression during Development Database, featuring advanced in-silico tools to characterize developmental lineages, investigate functional roles of temporally regulated genes, and compare developmental mechanisms across diverse species and life stages. This database integrates over 15 million cells from nine species, spanning 81 tissue-types and 42 time points, with three new analytical modules offered through an easy-to-use interface with dedicated cloud-based computational resources: (i) virtual gene knockout to assess transcriptome-wide responses to gene perturbation and their functional consequences; (ii) cross-species integration which minimizes species and data batch effects to reveal evolutionarily conserved and divergent temporal gene expression patterns; and (iii) trajectory inference and marker gene analysis to infer developmental lineages and detect marker genes relevant in cell fates decisions. Overall, this database provides researchers with a powerful platform to explore the temporal expression patterns of target genes, decipher finer regulation of developmental mechanisms, and guide both research design and discovery across development.