Journal of Genetics and Genomics

A turn from female gene to male determinant: evolutionary diversity and plasticity

Xi-Yin Li, Jian-Fang Gui

2026, 53(9): 1573-1574. doi: 10.1016/j.jgg.2026.07.004

Abstract (44)

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Cohesin variants associated with human reproductive and developmental disorders

Yuanyuan Liu, Jun Zhou

2026, 53(9): 1575-1584. doi: 10.1016/j.jgg.2026.04.024

Abstract (152)

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The cohesin complex is an evolutionarily conserved multi-subunit protein assembly essential for sister chromatid cohesion, meiotic recombination, DNA double-strand break repair, and transcriptional regulation. Pathogenic variants in its subunits are implicated in a spectrum of reproductive and developmental disorders, including non-obstructive azoospermia, premature ovarian insufficiency, reproductive aging, aneuploidy, Cornelia de Lange syndrome, Roberts syndrome, cancer, and neuropsychiatric disease. Consequently, identifying cohesin mutations is a priority for precision diagnostics and personalized medicine. This review systematically summarizes the cohesin variants linked to these pathologies, exploring their molecular mechanisms and clinical manifestations. A deeper understanding of these variants is crucial not only for deciphering disease etiology but also for guiding the development of targeted diagnostic strategies and therapeutic interventions, ultimately improving patient management and outcomes.

Plant nitrogen nutrition: enhancing plant resilience to abiotic stresses

Jinfei Zhang, Ying Liu, Shunan Zhang, Houqing Zeng, Wona Ding, Dajian Zhang, Guohua Xu

2026, 53(9): 1585-1598. doi: 10.1016/j.jgg.2026.03.004

Abstract (48)

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Nitrogen (N) is not only an essential macronutrient for plant growth and development but also functions as a pivotal signaling molecule that orchestrates adaptive responses to various abiotic stresses, including acidic stress, aluminum toxicity, salinity, drought, and extreme temperatures. This review synthesizes recent advances in our understanding of the molecular mechanisms by which N signaling, mediated by different N forms (e.g., NH₄⁺ and NO₃^-), integrates with core stress-response pathways. We specifically discuss the genetic crosstalk between N sensing and key signaling cascades, including abscisic acid (ABA) signaling, the salt overly sensitive (SOS) pathway, and reactive oxygen species (ROS) homeostasis. The review details how this integration modulates physiological and transcriptional reprogramming through central regulators such as NIN-like proteins (NLPs), calcineurin B-like protein (CBL)-interacting protein kinase (CIPK), and the target of rapamycin (TOR) kinase, ultimately optimizing the trade-off between growth and tolerance. By establishing a unified genetic and molecular framework, this review aims to provide a theoretical basis for developing novel strategies in precision N management and molecular breeding to synergistically enhance N use efficiency (NUE) and abiotic stress tolerance in crops.

Molecular mechanisms of plant thermal response: from signal transduction and epigenetic regulation to signaling integration

Huimin Ren, Hong Liu, Wenqiang Tang

2026, 53(9): 1599-1615. doi: 10.1016/j.jgg.2026.03.018

Abstract (215)

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Global warming intensification elevates heat stress to one of the major threats to crop productivity. This review synthesizes recent advances in understanding the mechanisms governing plant responses to both moderate and acute heat stress, with a focus on the integration of epigenetic regulation and signaling networks that underpin thermal adaptation. This review highlights how transcription factors PHYTOCHROME-INTERACTING FACTOR 4 (PIF4, during thermomorphogenesis) and HEAT SHOCK FACTOR A1s (HSFA1s, in heat shock responses) orchestrate plant adaptive growth through crosstalk among light, circadian, and hormone signaling pathways. Importantly, epigenetic mechanisms, including histone variant H2A.Z dynamics and histone modification reprogramming, function as central regulators of thermal plasticity. Key among these processes are HSFA2-mediated chromatin remodeling and small interfering RNA (siRNA)-dependent control of transgenerational thermomemory. Despite this progress, fundamental questions persist regarding temperature sensing, HSFA1s activation dynamics, and stress signal integration. Multi-omics and synthetic biology approaches are proposed to be pivotal in deciphering conserved principles of plant thermal resilience, ultimately providing a theoretical foundation and molecular breeding strategies for climate-smart crops.

A duplicated female pathway gene figla-like evolves as the male sex-determining gene in tilapia

Hesheng Xiao, Jingrong Wang, Yuhan Niu, Shuo Yan, Yang Zhang, Hanyuan Zhang, Zhen Xu, Baoyue Lu, Qianwen Min, Dejie Tan, Deshou Wang, Wenjing Tao

2026, 53(9): 1616-1630. doi: 10.1016/j.jgg.2026.05.001

Abstract (250)

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As the largest group of vertebrates, fish exhibit frequent turnover of sex-determining (SD) genes. Here, we assemble a chromosome-level YY red tilapia genome and identify figla-like (figlal) as the SD gene on tilapia linkage group (LG) 1. Integrative phylogenetic and genomic evidence suggests that figlal originated from a tilapia-specific duplication and transposition of the ancestral bHLH family gene figla from LG12 to LG1. Fluorescence in situ hybridization reveals expression divergence between figla and figlal, with figla expressed in female oocytes and figlal expressed in male gonadal somatic cells during early gonadal differentiation. The shift in expression after duplication might be driven by the insertion of cis-regulatory elements mediated by transposable elements. Knockout of figlal in XY fish results in male-to-female sex reversal as indicated by ovarian morphology, down-regulation of the male pathway gene dmrt1, and up-regulation of the female pathway gene cyp19a1a in the gonads. In contrast, overexpression of figlal in XX fish induces female-to-male sex reversal. These findings implicate figlal as an SD gene on tilapia LG1 and reveal the history of a unique evolutionary innovation in which a female oocyte gene evolved into a male SD gene via duplication, transposition, and cis-regulatory rewiring.

In vivo epigenome editing reduces circulating lipids and attenuates atherosclerosis in mice

Wei Wang, Yingjie Zhang, Lin Chen, Yuanbin Lu, Yunjie He, Hui Cheng, Ting Tang, Xinyi Li, Jiayi Zhang, Yan Liu, Yang Wang, Yuxuan Kong, Huijun Yuan

2026, 53(9): 1631-1644. doi: 10.1016/j.jgg.2026.04.004

Abstract (242)

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Atherosclerotic cardiovascular disease remains the leading cause of global mortality, with hypercholesterolemia serving as a critical driver of atherogenesis. Although current lipid-lowering therapies substantially improve circulating lipid profiles, strategies that provide more durable, safe, and efficient control of lipid metabolism are still needed. Epigenome editing offers a promising approach for long-lasting repression of disease-modifying genes without altering the underlying DNA sequence. Here, we develop CRISPRoff platforms delivered by adeno-associated virus or lipid nanoparticle to epigenetically silence hepatic Hmgcr or Pcsk9 in vivo. In both C57BL/6J wild-type and ApoE^-/- mice, CRISPRoff mediates robust and durable repression of these targets, leading to marked reductions in circulating total cholesterol, low-density lipoprotein cholesterol, and triglycerides. In the ApoE^-/- context, epigenetic silencing of Pcsk9 confers pronounced vascular protection, including decreased lipid accumulation in the liver and aortic root, reduced necrotic core formation, diminished macrophage infiltration, and enhanced plaque stability. Together, these results provide proof of principle that CRISPRoff-based epigenome editing enables stable repression of clinically relevant targets and ameliorates key features of atherosclerotic disease. This work lays the foundation for broader therapeutic applications of epigenetic modulation in cardiovascular disorders.

A single-nucleus transcriptome atlas of soybean anthers

Huangkai Zhou, Xiao Chen, Xinjing Yang, Tao Wu, Pengfei Ren, Yingying Tian, Javaid Akhter Bhat, Lin Weng, Ye Zhang, Diming Zhang, Genji Qin, Xuemei Chen, Xianzhong Feng

2026, 53(9): 1645-1661. doi: 10.1016/j.jgg.2026.03.006

Abstract (332)

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Anther development is crucial for plant sexual reproduction. However, a high-resolution, cell-type-specific transcriptomic atlas of this process is lacking for the legume crop soybean (Glycine max). Here, we construct a comprehensive transcriptional atlas of developing soybean anthers using single-nucleus RNA sequencing (snRNA-seq). We identify and characterize nine distinct cell types spanning both somatic and reproductive lineages. Our analysis reveals robust transcriptional continuity across anther developmental stages and dynamic reprogramming during key transitions. Notably, the shift from diploid meiocytes to haploid unicellular microspores is marked by the induction of previously inactive genes, despite an overall reduction in transcript abundance. Subsequently, within bicellular microspores, generative and vegetative cell lineages exhibit sharply divergent transcriptional programs: generative cells specialize in mRNA export and turnover, whereas vegetative cells up-regulate translational machinery. Evolutionary analysis further indicates that generative-cell-specific genes are subject to more relaxed purifying selection compared to those specific to vegetative cells. Functional validation using mutants generated by CRISPR/Cas9-mediated genome editing and EMS mutagenesis reveals the essential roles of OSD1A and PKSA in pollen development and fertility. This high-resolution atlas provides fundamental insights into the transcriptional regulation of soybean anther development and serves as a valuable resource for manipulating male fertility to advance hybrid breeding programs. The data are available at https://databases.genedenovo.com/pollen.

A single-nucleus and spatial transcriptomic atlas of poplar leaves reveals the regulation of leaf polarity and cuticle deposition

Yiling Li, Lingfei Kong, Xing Guo, Yang Chen, Wenwen Shao, Min Liu, Chenmeng Luo, Shaoming Liang, Ao Feng, Li Xu, Huan Liu, Tong Wei, Yuanzhong Jiang, Tao Ma

2026, 53(9): 1662-1676. doi: 10.1016/j.jgg.2026.03.015

Abstract (311)

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Leaf adaxial-abaxial polarity is fundamental for plant morphogenesis and environmental adaptation through asymmetric cell differentiation. Emerging evidence reveals dorsoventral metabolic gradients act downstream of transcriptional networks to fine-tune cellular specialization. While conserved transcription factors (e.g., HD-ZIP III and KANADI) establish initial polarity, the molecular networks driving position-specific cellular differentiation and their integration with metabolic adaptation remain unclear. Leveraging single-nucleus and spatial transcriptomics, we resolve major cell classes (mesophyll, epidermal, and vascular-associated) and their adaxial-abaxial subtypes, revealing dorsoventral polarity in transcriptional profiles and metabolic pathways. Adaxial cells are enriched in phenylpropanoid/flavonoid biosynthesis, while abaxial cells show preferential activation of stress and hormone signaling. Notably, we identify MYC2 as a key regulator of adaxial cuticle biosynthesis, binding to promoters of lipid biosynthetic and transport genes (e.g., CER10 and LTPG1) and promoting cuticle thickening. Our study uncovers how positional identity shapes transcriptional and metabolic polarity in leaves, with MYC2 emerging as a central regulator coordinating organ-specific adaptations. These findings provide insights into the spatial regulation of plant development and stress resilience, offering potential strategies for engineering stress-tolerant woody crops.

Metabolome-based genome-wide association study provides genetic insights into the andrographolide accumulation in Andrographis paniculata

Yuxia Wang, Xu Li, Bin Jin, Jiawen Chen, Duan Wu, Qi Shen

2026, 53(9): 1677-1687. doi: 10.1016/j.jgg.2026.03.013

Abstract (172)

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Andrographis paniculata is a distinctive medicinal plant that produces andrographolide-related metabolites, a class of diterpenoid compounds with potent anti-inflammatory activities. To elucidate the genetic mechanisms underlying the biosynthesis of these compounds, we perform comprehensive metabolic profiling and whole-genome resequencing on a natural population of A. paniculata. Population structure analysis reveals four distinct subgroups characterized by low intra-group genetic diversity but significant inter-group differentiation. Through metabolome-based genome-wide association study, we identify a significant locus associated with 14-deoxyandrographolide content. This locus harbors the candidate gene ApNB-ARC25 (CXN00004106), which encodes an NB-ARC domain-containing resistance protein. Functional characterization using virus-induced gene silencing shows that silencing of ApNB-ARC25 significantly reduces andrographolide accumulation and downregulates expressions of key genes in the andrographolide biosynthetic pathway. Heterologous overexpression of ApNB-ARC25 in rice not only improves resistance to blast disease but also enhances diterpenoid phytoalexin production. Our findings reveal that ApNB-ARC25 promotes diterpenoid accumulation and andrographolide biosynthesis by upregulating key genes involved in terpenoid backbone formation and diterpenoid synthesis. This work not only expands the functional understanding of the ApNB-ARC gene family but also provides a genetic resource for enhancing valuable compound accumulation in medicinal plants, offering important insights into the molecular regulation of medicinal metabolite biosynthesis.

Probiotic potential of Parabacteroides johnsonii in mitigating age-related ovarian functional decline

Dan-Yang Wang, Yin-Wei Wang, Ke-Chun Yu, Xuan Yang, Jun Ma, Bo-Han Li, Ya-Ling Peng, Xin-Yin Deng, Zhen-Xia Chen, Ling Wang

2026, 53(9): 1688-1702. doi: 10.1016/j.jgg.2026.03.023

Abstract (193)

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The gut microbiota is increasingly recognized as a regulator of reproductive health, yet its role in ovarian aging remains unclear. Here, we combine Mendelian randomization (MR) analysis with experimental validation to investigate the causal relationship between gut microbiota and ovarian aging. MR analysis identifies four microbial taxa significantly associated with age at natural menopause. In mouse models, germ-free mice exhibit accelerated ovarian functional decline, including reduced ovarian reserve and impaired folliculogenesis. Fecal microbiota transplantation (FMT) from young donors alleviates ovarian aging phenotypes, whereas FMT from aged donors exacerbates functional decline. Metagenomic analysis reveals species-level differences between young and ovarian-aging mice, with Parabacteroides johnsonii (P. johnsonii) enriched in young mice. Administration of P. johnsonii to middle-aged mice improves ovarian reserve, reduces follicular atresia, enhances granulosa cell proliferation, and decreases systemic inflammation. These findings highlight a causal role of the gut microbiota in ovarian aging and support microbiota-targeted interventions as a potential strategy to preserve ovarian function.

Chromatin-binding protein HMGN1 promotes HCC tumorigenesis via histone methylation-induced RALB transcriptional suppression

Xiameng Su, Leirong Gu, Tingting Gao, Wanjin Chen, Ming Tan, Yuting Liu, Zhiling Wang, Xinyan Chen, Hui Zhang, Shengtao Cheng

2026, 53(9): 1703-1717. doi: 10.1016/j.jgg.2026.03.009

Abstract (155)

Abstract:
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide, with metastasis being the primary cause of its high mortality. The chromatin-binding protein, high mobility group nucleosome binding domain 1 (HMGN1), has been implicated in tumour progression, but its specific role and mechanism in HCC metastasis remain unclear. This study investigates the function of HMGN1 and its potential as a therapeutic target. Analysis of patient samples confirms an upregulation of HMGN1 in HCC tissues, correlating with advanced disease and poor prognosis. Functional assays demonstrate that HMGN1 promotes HCC metastasis in vitro and in vivo. Mechanistically, integrated RNA sequencing and chromatin immunoprecipitation sequencing analyses reveal that HMGN1 binds to the promoter of RAS-like proto-oncogene B (RALB) gene, recruiting the repressive histone mark H3K9me2 to epigenetically silence its transcription and drive metastasis. Therapeutically, a nanoparticle delivery system for siRNA against HMGN1 effectively silences its expression and inhibits metastasis in orthotopic liver xenograft tumour models. Our findings establish HMGN1 as a key epigenetic driver of HCC metastasis and highlight siRNA-nanoparticle targeting of HMGN1 as a promising precision therapeutic strategy.

Sex-specific regulation of SLC39A11 in the murine liver

Xiaopeng Li, Yanhan Feng, Biyao Tang, Enjun Xie, Jiaming Wang, Junxia Min, Fudi Wang, Zhidan Xia

2026, 53(9): 1718-1730. doi: 10.1016/j.jgg.2026.04.003

Abstract (50)

Abstract:
Sex differences in health and disease are evident in humans and many other animal species. However, the sex-related determinants are less understood, and the underlying mechanisms remain elusive. By analyzing the RNA-seq data, we unexpectedly find that Slc39a11 is significantly associated with the non-alcoholic fatty liver disease pathway only in female mice, revealing a sex-specific role of Slc39a11 in liver metabolism. We then generate tissue-specific SLC39A11 knock-in and Slc39a11 knockout mice and find that female but not male SLC39A11-liver conditional overexpression (LKI) mice develop more severe cholestasis and liver injury compared to controls when fed a methionine/choline-deficient (MCD) diet. In contrast, female Slc39a11-liver conditional knockout (LKO) mice exhibit attenuated liver injury under MCD feeding. Ovariectomy in female mice largely reversed these phenotypes. Interestingly, female SLC39A11-intestine-specific overexpression (IKI) mice show alleviated liver damage, whereas female Slc39a11-intestine-specific knockout (IKO) mice develop exacerbated liver injury under MCD feeding; these effects are not observed in male SLC39A11-IKI or Slc39a11-IKO mice. This study reveals that SLC39A11 regulates liver metabolism both intrinsically and via the gut-liver axis through an evolutionarily conserved, sexual dimorphism mechanism, partially involving estrogen signaling and manganese metabolism, suggesting SLC39A11 is a potential target for the diagnosis and treatment of hepatobiliary diseases.

pKAKA: a protein language model for prioritizing kinase-disrupting variants in diseases

Jun-Teng Li, Haoyang Cheng, Zhuoran Liang, Jiamin Hu, Yi Chu, Ruoxi Cai, Bijin Cao, Ying Jin, Yu-Xi Xie, Huai-Qiang Ju, Linyan Li, Yaping Guo, Ze-Xian Liu

2026, 53(9): 1731-1746. doi: 10.1016/j.jgg.2026.03.010

Abstract (157)

Abstract:
Protein kinases are pivotal regulators of cellular signaling, and their genetic variations are frequently implicated in diseases. Although numerous kinase mutations have been identified as drivers of altered activity, with a few successfully targeted therapeutically, the functional impact of most variants remains uncharacterized. To bridge this gap, we curate a comprehensive dataset that contains 2553 experimentally validated kinase activity-related key alterations (KAKAs) from the literature. While many mutations outside canonical functional regions are known to affect kinase activity, systematic methods to predict their functional consequences are lacking. Consequently, we develop a computational method to predict potential KAKAs, leveraging transfer learning on the pre-trained protein language model ProtBert. Our model, termed pKAKA, achieves an impressive AUC score of 0.9593 and outperforms the AlphaMissense benchmark in comparative testing. Systematic analysis of kinase missense mutations underscores the critical role of KAKAs in pathogenesis, with highlights including JAK2 V617F in atherosclerotic cardiovascular disease, LRRK2 G2385R in Parkinson's disease, EGFR L858R in lung adenocarcinoma, and EGFR G598V in glioma. Overall, this study significantly advances our understanding of how mutations that influence kinase activity contribute to disease mechanisms.

A FERONIA-MPK3/6-WRKY3/4 module links auxin signaling to lateral root development in Arabidopsis

Weiwei Ren, Hongxia Zheng, Yueyue Li, Gaojian Li, Lili Zhang, Zhen Wu, Meihong Sun, Yuhong Zhang, Shaojun Dai

2026, 53(9): 1747-1759. doi: 10.1016/j.jgg.2026.03.017

Abstract (224)

Abstract:
The phytohormone auxin orchestrates root development through intricate signaling networks. In the non-canonical auxin pathway, both the transmembrane kinase (TMK)-mediated signaling and the mitogen-activated protein kinase (MAPK) cascade are shown to be involved in the auxin-regulated lateral root (LR) formation. However, the role and mechanism of the receptor-like kinase FERONIA (FER) in this process remain unclear. Here, quantitative proteomic and phosphoproteomic analyses of Arabidopsis roots identify FER, MPK3/6, and WRKY3/4 as auxin-responsive components. Further analyses reveal that FER functions as a negative regulator of LR development by modulating cell division patterns within LR primordia. FER interacts with and phosphorylates MPK3/6, which then phosphorylate the transcription factors WRKY3 and WRKY4 to form a repressive module that ultimately suppresses LR organogenesis. Collectively, our findings define a FER-MPK3/6-WRKY3/4 signaling module that negatively regulates LR formation, demonstrating a previously unknown integration of FER-mediated signaling into the MAPK cascade in auxin-triggered organogenesis.

Phosphorylation and ubiquitination coordinate homeostasis of a tomato transporter responsible for fruit sugar accumulation

Bangqian Song, Yong Kang, Xi Zheng, Zhengguo Li, Yulin Cheng

2026, 53(9): 1760-1772. doi: 10.1016/j.jgg.2026.03.019

Abstract (152)

Abstract:
Sugar transport mediated by different transporters is essential for maintaining sugar homeostasis in plants. Here, we report that phosphorylation and ubiquitination coordinate the homeostasis of a tomato (Solanum lycopersicum) sugar transporter SlSWEET16, revealing a new aspect of plant sugar homeostasis. SlSWEET16 is localized to plasma membrane and functions as a mono- and disaccharide transporter. SlSWEET16 mediates cellular sugar efflux, and CRISPR/Cas9-mediated knockout of SlSWEET16 leads to increased fruit sugar accumulation. Strikingly, the C-terminus of SlSWEET16 is subjected to both phosphorylation and ubiquitination. Two protein kinases including SlSnRK2.3 and SlSnRK2.4 associate with the C-terminus of SlSWEET16, resulting into an increase in the stability of SlSWEET16. Meanwhile, the C-terminus of SlSWEET16 also interacts with an E3 ubiquitin ligase SlTT3.1L2, which decreases the stability of SlSWEET16. SlSnRK2.3 and SlSnRK2.4 inhibit fruit sugar accumulation, whereas SlTT3.1L2 promotes it. Mutations of phosphorylated or ubiquitinated residues in SlSWEET16's C-terminus further corroborate the contribution of phosphorylation and ubiquitination to the stability of SlSWEET16 and fruit sugar accumulation. Our results reveal a multiple-protein regulatory module that integrates different post-translational modifications to control transporter-mediated fruit sugar accumulation.

Natural variation in Miniature5 determines mitochondrial nad1 splicing and seed development in maize

Yuyu Wang, Rongrong Li, Jiajia Deng, Lizhen Wang, Zhiyi Tang, Jiahui Li, Yingbin Mu, Mingliang Yang, Fan Wu, Jie Lei, Xiaoyue Luan, Hongyu Chen, Jihua Tang, Qingwen Shen, Guifeng Wang

2026, 53(9): 1773-1787. doi: 10.1016/j.jgg.2026.03.021

Abstract (151)

Abstract:
Seed size is a key determinant of cereal grain yield, but natural variations in defective-kernel genes have rarely been applied in maize breeding. Here, we report the positional cloning of maize Miniature5 (Mn5), which encodes a mitochondrial-targeted P-class pentatricopeptide repeat (PPR) protein. Further analysis shows that a missense mutation of Mn5, Mn5^Val109, presents in maize populations and correlates with reduced seed size. The Mn5^Val109 variant exhibits compromised function in the miniature5 (mn5-ref) mutant, failing to trans-splice mitochondrial nad1 intron1, drastically reducing the abundance and activity of respiratory complex I, accompanied by disorganized mitochondrial cristae. Mn5 directly binds to domain IV of the pre-nad1.1 transcript. Notably, this binding site is located downstream of the previously presumed 3′-terminus bound by MITOCHONDRIA STABILITY/PROCESSING PPR FACTOR1 (MSP1), thus redefining the 3′-end of the nad1.1 pre-RNA. Furthermore, Mn5 physically interacts with the maturases ZmnMAT1 and ZmnMAT3, as well as the PPR proteins PPR-SMR1 and SPR2, which are broadly involved in organellar group II intron splicing. Together, our results suggest that Mn5 recruits maturases and PPR proteins to form spliceosomal complexes responsible for the trans-splicing of nad1 intron1. Importantly, natural variations in Mn5 confer differences in seed size control, offering potential for breeding high-yield maize varieties.

Single-nucleotide transcription start sites profiling via Nascent Strand-Specific RNA sequencing uncovers IFN-γ-induced promoter dynamics

Ke Sun, Luemou Shen, Junli Wang, Jiahao Zheng, Xu Zhang, Fucheng Luo, Kai Chen, Ning Song

2026, 53(9): 1788-1799. doi: 10.1016/j.jgg.2026.03.014

Abstract (191)

Abstract:
Transcriptional regulation is a highly dynamic process in which nascent RNAs provide the most immediate readout of transcriptional activity. Precise mapping of transcription start sites (TSSs) is therefore critical for understanding promoter architecture and gene regulation, yet remains technically challenging. Here, we introduce Nascent Strand-Specific RNA sequencing (NSS-seq), a robust and streamlined method for genome-wide profiling of the capped 5′ ends of nascent RNAs. By directly capturing transcription initiation events, NSS-seq overcomes the temporal delay inherent to conventional RNA-seq and enables time-resolved interrogation of transcriptional dynamics. Applied to interferon-γ (IFN-γ)-stimulation, NSS-seq uncovers previously unrecognized IFN-γ-responsive genes and transient transcription factor activation patterns underlying interferon-mediated tumor-suppressive functions. Together, NSS-seq provides a cost-effective and technically accessible platform for dissecting promoter-level regulatory dynamics during cellular responses.

Precision-edited D9 allele breaks the trade-off between maize dwarfing and yield