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Histone 3 Lys 27 trimethylation (H3K27me3)-mediated epigenetic silencing plays a critical role in multiple biological processes. However, the H3K27me3 recognition and transcriptional repression mechanisms are only partially understood. Here, we report a mechanism for H3K27me3 recognition and transcriptional repression. Our structural and biochemical data showed that the BAH domain protein AIPP3 and the PHD proteins AIPP2 and PAIPP2 cooperate to read H3K27me3 and unmodified H3K4 histone marks, respectively, in Arabidopsis . The BAH-PHD bivalent histone reader complex silences a substantial subset of H3K27me3-enriched loci, including a number of development and stress response-related genes such as the RNA silencing effector gene ARGONAUTE 5 ( AGO5 ). We found that the BAH-PHD module associates with CPL2, a plant-specific Pol II carboxyl terminal domain (CTD) phosphatase, to form the BAH-PHD-CPL2 complex (BPC) for transcriptional repression. The BPC complex represses transcription through CPL2-mediated CTD dephosphorylation, thereby causing inhibition of Pol II release from the transcriptional start site. Our work reveals a mechanism coupling H3K27me3 recognition with transcriptional repression through the alteration of Pol II phosphorylation states, thereby contributing to our understanding of the mechanism of H3K27me3-dependent silencing. Histone 3 Lys 27 trimethylation (H3K27me3) mediates epigenetic silencing of gene expression. Here, Zhang et al. show that in Arabidopsis, the BAH-domain H3K27me3-reader protein AIPP3 forms a complex with PHD proteins and CPL2, a plant-specific Pol II phosphatase, to inhibit Pol II activity by dephosphorylation.

Existing multi-style image generation methods face critical challenges: insufficient content-style decoupling, high computational costs for high-resolution generation, and structural distortion during style transfer. To address these, we propose the Dual-Conditional Lightweight Style Diffusion Model (DCLSDM), a novel approach enhancing content-style decoupling via a dual-conditional control mechanism. This mechanism independently manages content structure and style expression, enabling better control in style transfer. Experimental results on WikiArt and Summer2Winter Yosemite datasets show DCLSDM outperforms comparative models in SSIM, LPIPS, and FID, with significant improvements in inference time, memory usage, and parameter scale–making it suitable for resource-constrained scenarios. It offers an efficient, controllable solution for multi-style image generation, with potential in content creation and digital art production.

The unfolded protein response (UPR) signaling network encompasses two pathways in plants, one mediated by inositol-requiring protein-1 (IRE1)-bZIP60 mRNA and the other by site-1/site-2 proteases (S1P/S2P)-bZIP17/bZIP28. As the major sensor of UPR in eukaryotes, IRE1, in response to endoplasmic reticulum (ER) stress, catalyzes the unconventional splicing of HAC1 in yeast, bZIP60 in plants and XBP1 in metazoans. Recent studies suggest that IRE1p and HAC1 mRNA, the only UPR pathway found in yeast, evolves as a cognate system responsible for the robust UPR induction. However, the functional connectivity of IRE1 and its splicing target in multicellular eukaryotes as well as the degree of conservation of IRE1 downstream signaling effectors across eukaryotes remains to be established. Here, we report that IRE1 and its substrate bZIP60 function as a strictly cognate enzyme-substrate pair to control viral pathogenesis in plants. Moreover, we show that the S1P/S2P-bZIP17/bZIP28 pathway, the other known branch of UPR in plants, does not play a detectable role in virus infection, demonstrating the distinct function of the IRE1-bZIP60 pathway in plants. Furthermore, we provide evidence that bZIP60 and HAC1, products of the enzyme-substrate duet, rather than IRE1, are functionally replaceable to cope with ER stress in yeast. Taken together, we conclude that the downstream signaling of the IRE1-mediated splicing is evolutionarily conserved in yeast and plants, and that the IRE1-bZIP60 UPR pathway not only confers overlapping functions with the other UPR branch in fundamental biology but also may exert a unique role in certain biological processes such as virus-plant interactions.

• Autophagy is an evolutionarily conserved pathway in eukaryotes that delivers unwanted cytoplasmic materials to the lysosome/vacuole for degradation/recycling. Stimulated autophagy emerges as an integral part of plant immunity against intracellular pathogens. • In this study, we used turnip mosaic virus (TuMV) as a model to investigate the involvement of autophagy in plant RNA virus infection. • The small integral membrane protein 6K2 of TuMV, known as a marker of the virus replication site and an elicitor of the unfolded protein response (UPR), upregulates the selective autophagy receptor gene NBR1 in a UPR-dependent manner. NBR1 interacts with TuMV NIb, the RNA-dependent RNA polymerase of the virus replication complex (VRC), and the autophagy cargo receptor/adaptor protein ATG8f. The NIb/NBR1/ATG8f interaction complexes colocalise with the 6K2-stained VRC. Overexpression of NBR1 or ATG8f enhances TuMV replication, and deficiency of NBR1 or ATG8f inhibits virus infection. In addition, ATG8f interacts with the tonoplast-specific protein TIP1 and the NBR1/ATG8f-containing VRC is enclosed by the TIP1-labelled tonoplast. In TuMV-infected cells, numerous membrane-bound viral particles are evident in the vacuole. • Altogether these results suggest that TuMV activates and manipulates UPR-dependent NBR1-ATG8f autophagy to target the VRC to the tonoplast to promote viral replication and virion accumulation.

This paper investigates gender differentials in citations of articles published between 2003 and 2014 in two journals specialized in Demographic Economics, the Journal of Population Economics (JPOP) and the Review of Economics of the Household (REHO). We utilize different definitions of authorship. Articles with female corresponding authors receive 24% more citations than articles with male corresponding authors. Citations go up by 36% when there is a female co-author. We did not detect any significant associations between citations and male co-authors. In addition, citations go up with the proportion of female authors. We discuss some potential explanations for our findings.

Recent studies have suggested that ultraviolet-C (UV-C) overexposure induces programmed cell death (PCD) in Arabidopsis thaliana (L.) Heynh, and this process includes participation of caspase-like proteases, DNA laddering as well as fragmentation of the nucleus. To investigate possible early signal events, we used microscopic observations to monitor in vivo the behaviour of mitochondria, as well as the production and localization of reactive oxygen species (ROS) during protoplast PCD induced by UV-C. A quick burst of ROS was detected when the protoplasts were kept in continuous light after UV-C exposure, which was restricted in chloroplasts and the adjacent mitochondria. Pre-incubation with ascorbic acid (AsA, antioxidant molecule) or 3-(3, 4-dichlorophenyl)-1, 1-dimethylurea (DCMU, an inhibitor of photosynthetic electron transport) decreased the ROS production and partially protected protoplasts from PCD. A mitochondrial transmembrane potential (MTP) loss occurred prior to cell death; thereafter, the mitochondria irregularly clumped around chloroplasts or aggregated in other places within the cytoplasm, and the movement of mitochondria was concomitantly blocked. Pre-treatment with an inhibitor of mitochondrial permeability transition pores (MPTP), cyclosporine (CsA), effectively retarded the decrease of MTP and reduced the percentage of protoplasts undergoing PCD after UV-C overexposure. Our results suggest that the MTP loss and the changes in distribution and mobility of mitochondria, as well as the production of ROS play important roles during UV-induced plant PCD, which is in good accordance with what has been reported in many types of apoptotic cell death, both in animals and plants.

Maintaining genomic integrity and faithful transmission of genetic information is essential for the survival and proliferation of cells and organisms. DNA damage, which threatens the integrity of the genome, is rapidly sensed and repaired by mechanisms collectively known as the DNA damage response. The RNA demethylase FTO has been implicated in this process; however, the underlying mechanism by which FTO regulates DNA repair remains unclear. Here, we use an unbiased quantitative proteomic approach to identify the proximal interactome of endogenous FTO protein. Our results demonstrate a direct interaction with the DNA damage sensor protein PARP1, which dissociates upon ultraviolet stimulation. FTO inhibits PARP1 catalytic activity and controls its clustering in the nucleolus. Loss of FTO enhances PARP1 enzymatic activity and the rate of PARP1 recruitment to DNA damage sites, accelerating DNA repair and promoting cell survival. Interestingly, FTO regulates PARP1 function and DNA damage response independent of its catalytic activity. We conclude that FTO is an endogenous negative regulator of PARP1 and the DNA damage response in cells beyond its role as an RNA demethylase. Maintaining genomic integrity is essential for the survival of organisms. Here, the authors identify FTO as an endogenous negative regulator of PARP1 and the DNA damage response in cells beyond its role as an RNA demethylase.

Functionalized benzosultam and sulfonamide derivatives represent privileged pharmacophores in medicinal chemistry. However, noncanonical amino acids (ncAAs) featuring benzosultam side chains remain underexplored for peptide therapeutics, despite significant advances in peptide drug development. Herein, we report the promiscuous activity of the PLP‐dependent decarboxylative aldolase UstD in catalyzing β‐Mannich reactions. An engineered variant, UstD2.0S60A, was developed and applied to synthesize 23 enantioenriched ncAAs, achieving yields up to 96%, a total turnover number (TTN) of 7500, and excellent stereoselectivity (>95:5 dr, >99:1 er). The reaction is scalable to gram quantities for preparative applications. This study facilitates the future use of benzosultam‐containing ncAAs in peptide chemistry and highlights the opportunity of engineering aldolases for non‐natural Mannich reaction to access chiral amine products. The pyridoxal 5′‐phosphate dependent decarboxylative aldolase, UstD was engineered to catalyze a Mannich reaction with cyclic imines. This enzymatic route was applied to synthesize 23 enantioenriched noncanonical amino acids with benzosultam side chains, achieving yields up to 96%, a total turnover number (TTN) of 7500, and excellent stereoselectivity (>95:5 d.r., >99:1 e.r.).

Heat shock transcription factor A2 (HsfA2) participates in multiple stress responses. To provide new insights into the role of HsfA2 in the heat stress (HS) response, in vivo production and localization of reactive oxygen species (ROS) and mitochondrial dynamics were investigated during the onset of cell death induced by an HS (40 °C, 10 min) applied after a 2 d recovery at 24 °C following a conditioning treatment at 37 °C for 1 h. In response to the HS, generated ROS were significantly higher in hsfA2 than in wild-type (WT) protoplasts and did not return to the baseline level when compared with WT protoplasts. The uncontrolled ROS in hsfA2 protoplasts localized not only to mitochondria but also to chloroplasts. Microscopic observations also revealed that, prior to cell death, hsfA2 protoplasts underwent more severe alterations in mitochondrial dynamics than WT protoplasts, including mitochondrial swelling, transmembrane potential loss, and the cessation of mitochondrial movement. The lower cell viability in hsfA2 than in WT protoplasts suggested that--combined with the findings that antioxidants only partially blocked ROS generation and arrested cell death in hsfA2 protoplasts relative to WT protoplasts--ROS participated in HS-induced cell death. Also the disruption of HsfA2 resulted in more severe oxidative stress and more cell death which, together with the more severe alterations in mitochondrial dynamics, could be complemented by introducing a WT copy of HsfA2. These results represent the first subcellular evidence that HsfA2 protects plants against HS-induced oxidative damage, organelle dysfunction, and subsequent cell death.

Epigenome and cis‐regulome, comprising cis‐regulatory elements (CREs) and modules (CRMs), jointly define the architecture of gene regulation. However, the causal mechanisms by which epigenetic marks influence CRM function remain elusive. To address this, modular epigenome editing frameworks, exemplified by dead Cas9‐coupled DNA demethylation (dCd) and DNA methylation (dCm) platforms, are developed for programmable dissection and engineering of CRM activity. The dCd system modulates methylation levels and transcriptional output at CRMs in situ or ex situ, in accordance with CRM‐specific methylation responsiveness, and alters co‐transcriptional RNA processing to yield predictable phenotypic outcomes in plants. These findings underscore the reliability of targeted DNA demethylation. In parallel, the dCm system reconstitutes methylation‐dependent and ‐sensitive CRMs of diverse origins in Saccharomyces cerevisiae, a species devoid of native DNA methylation, enabling causal dissection of epigenetic regulation and revealing cross‐species portability. This system further uncovers crosstalk between DNA methylation and chromatin modifications, and enables logic‐gated control of endogenous genes through CRM engineering. Incorporation of optogenetic and temperature‐sensitive anti‐CRISPR inhibitors confers tunable, reversible regulation, proposing dCm as a foundation for input‐responsive synthetic epigenome editors. Together, these frameworks provide a versatile platform to decode and reprogram cis‐regulatory epigenetic logic, with broad applications in trait design and synthetic biology. Epigenome editing surpasses genome editing in gene regulation. Modular epigenome editing frameworks are developed to interrogate cis‐regulome, enabling tunable reprogramming of cis‐elements, uncovering their epigenetic responsiveness and cross‐species portability. Informed by these new insights, a plant‐specific “methylstat” powers engineering in non‐DNA‐methylating yeast, achieving logic‐gated epigenetic control of endogenous genes and opening a new dimension in circuit design for synthetic biology.