Journal of Genetics and Genomics

Advances in monogenic female infertility

Hao Gu, Lei Wang, Qing Sang

2026, 53(4): 555-576. doi: 10.1016/j.jgg.2025.11.009

Abstract (0)

Abstract:
Human reproduction requires the fertilization of a mature oocyte with a sperm to form a high-quality embryo. Oogenesis, folliculogenesis, and the activities of the endocrine system play essential roles in female fertility, and disturbances in these processes can result in female infertility, which has become an urgent public health issue worldwide. Genetic studies have identified multiple variants in key genes underlying these processes in infertile females, and these patients are mainly diagnosed with disorders of sex development, premature ovarian insufficiency, congenital hypogonadotropic hypogonadism, central precocious puberty, resistant ovary syndrome, oocyte maturation arrest, fertilization failure, and early embryonic defects. Notably, the known genes account for about 13.2% cases of oocyte and embryo defects (479/3627) and 18.7% cases of premature ovarian insufficiency (193/1030). Here, we review the critical events in female reproduction and highlight the single gene variants with Mendelian inheritance patterns that are responsible for female infertility.

The role of primary cilia in physiological and pathological states of the central nervous system

Denghui Zhai, Xuebin Zhou, Zhangqi Xu, Xiying Chen, Ya Li, Jiabin Li, Tianhua Zhou, Shanshan Xie

2026, 53(4): 577-593. doi: 10.1016/j.jgg.2025.11.011

Abstract (54) PDF (2)

Abstract:
Primary cilia, microtubule-based organelles widely existing on eukaryotic cells, play a critical, indispensable role in the development and functional maintenance of the central nervous system (CNS). Here, we summarize recent advances on the distribution of primary cilia across different regions of the CNS, providing a detailed map highlighting their presence on both neurons and glial cells. Furthermore, we elaborate on the roles of primary cilia in essential physiological functions, including progenitor cell proliferation, neurogenesis, neuronal migration, and synaptic connections within the CNS. We also discuss the emerging links between ciliary dysfunction and a range of CNS disorders, including cognitive impairment, metabolic disorders and hyperphagia-induced obesity, neurodegenerative diseases, and psychiatric conditions. Integrating existing findings, this review provides a panoramic perspective on ciliary roles in the CNS and lays a critical foundation for subsequent basic research, disease-mechanism studies, and therapeutic-target exploration.

Roles of ethylene in plant growth, development, and stress responses

Xun Zhang, Jianjun Tao, Yihua Huang, Shouyi Chen, Cuicui Yin, Jinsong Zhang

2026, 53(4): 594-614. doi: 10.1016/j.jgg.2025.11.015

Abstract (0) PDF (0)

Abstract:
Ethylene, a pivotal gaseous phytohormone, regulates diverse processes in plant growth, development, and stress adaptation. In Arabidopsis (Arabidopsis thaliana), ethylene perception by endoplasmic reticulum localized receptors initiates a canonical signaling cascade involving CONSTITUTIVE TRIPLE RESPONSE 1 (AtCTR1) and ETHYLENE INSENSITIVE 2 (AtEIN2). This pathway culminates in nuclear translocation of AtEIN2-CEND and activation of the transcription factor AtEIN3/EIN3-LIKE1 (AtEIL1). Rice employs conserved (OsEIN2, OsCTR2, OsEIL1/2) and unique (Mao Huzi 3 [MHZ3], MHZ11, MHZ1) components for ethylene signaling, reflecting adaptations to semi-aquatic environments. Ethylene regulates developmental processes including seed germination, apical hook formation, root architecture, flowering, and senescence, often via intricate crosstalk with auxin, abscisic acid, jasmonic acid, gibberellins, and brassinosteroids. Ethylene signaling also influences rice yield-related traits such as grain filling, grain size, and starch biosynthesis. Moreover, ethylene modulates responses to abiotic stresses (such as submergence, hypoxia, salinity, drought, and temperature fluctuations) and nutrient imbalances. This review synthesizes current understanding of ethylene signaling and its functions, focusing on the model dicot Arabidopsis and the monocot rice (Oryza sativa). It highlights conserved and diverged mechanisms, underscoring ethylene's potential as a target for enhancing crop resilience and productivity in changing environments.

MEI4 variations drive female reproductive disorders via impaired oocyte abundance and developmental potential

Yiyang Wang, Yu Qi, Keyan Xu, Shuyan Tang, Luyi Tan, Bingying Xu, Ying Wang, Shuxian Zhang, Yang Zou, Yuan Gao, Chunmei Zhang, Xin Liang, Xue Jiao, Shidou Zhao, Han Zhao, Shixuan Wang, Yingying Qin, Ting Guo, Zi-Jiang Chen

2026, 53(4): 615-629. doi: 10.1016/j.jgg.2025.12.005

Abstract (0)

Abstract:
Meiotic DNA double-strand break (DSB) formation is pivotal for oocyte development, regulating both ovarian reserve and oocyte developmental potential. Mutations in DSB formation genes have been associated with premature ovarian insufficiency (POI) and adverse pregnancy outcomes in women. Whole exome sequencing in 1530 POI patients across two Chinese cohorts identifies loss-of-function variants in the DSB formation gene, MEI4, enriched in POI. These MEI4 variants impair DSB formation in vitro and reveal a previously unrecognized function of the MEI4 C-terminus in stabilizing the MEI4–REC114 subcomplex on the chromosome axes. Additionally, Mei4^{Arg356∗/Arg356∗} mice display severe defects in DSB formation, leading to massive apoptosis in oocytes triggered by the HORMAD1-dependent synapsis checkpoint in late prophase I. The few mutant oocytes surviving past the checkpoint exhibit low developmental potential, characterized by complete early embryonic arrest due to aneuploidy. Notably, heterozygous Mei4^+/Arg356∗ mice show intermediate follicle depletion and embryonic development arrest consistent with the phenotype of heterozygous POI and preimplantation embryonic arrest, suggesting a haploinsufficiency effect. This study defines the impacts of MEI4 mutation on oocyte quantity and quality, which can guide genetic diagnosis and intervention in patients with POI and early embryonic arrest, especially those with mutations in meiotic DSB formation genes.

Epigenetic regulation of cilia stability and kidney development by the SWI/SNF chromatin remodeling complex in zebrafish

Xiaoyu Cheng, Qianshu Zhu, Shilin Ma, Xiaoyu Peng, Guanliang Huang, Guifen Liu, Wentao Zhang, Yong Zhang, Cizhong Jiang, Andong Qiu, Ying Cao

2026, 53(4): 630-642. doi: 10.1016/j.jgg.2025.11.001

Abstract (66)

Abstract:
Cilia are vital subcellular organelles whose assembly is regulated by master transcription factors, such as Foxj1 and Rfx. However, the mechanisms of epigenetic regulation over cilia stability remain largely unclear. Here, we investigate epigenetic control by manipulating chromatin-remodeling genes in zebrafish. We demonstrate that the depletion of multiple components of the switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex induces ciliopathy-like phenotypes in zebrafish embryos. Specifically, the loss of Actl6a, an essential component of the SWI/SNF complex, leads to cilia disassembly and cystic kidney defects, without affecting ciliary motility. Our multi-omics analyses (RNA-seq, ATAC-seq, and FitCUT&RUN) consistently reveal that in Actl6a-depleted pronephros or embryos, a critical set of ciliary genes, including the master regulators foxj1a and rfx2, exhibit concordant downregulation across the transcriptional level, chromatin accessibility, and SWI/SNF binding. Consistently, the depletion of foxj1a or rfx2 causes cilia assembly defects and cystic kidney formation in zebrafish. Furthermore, overexpression of either foxj1a or rfx2 mRNA substantially rescues the cystic kidney and cilia disassembly defects observed in actl6a^−/− mutant embryos. Collectively, these findings reveal that the SWI/SNF complex maintains cilia stability and kidney homeostasis by directly modulating the expression of the key ciliogenesis transcription factors foxj1a and rfx2.

Genome-wide association study of HBV-related hepatocellular carcinoma identifies a functional variant at the FAM114A1 locus

Hong-Ping Yu, Bang-De Xiang, Ji Qian, Hongliang Liu, Yuan-Feng Li, Qiuling Lin, Shun Liu, Junjie Wei, Shicheng Zhan, Binbin Jiang, Juncheng Dai, Liang Ma, Litu Zhang, Yingchun Liu, Qiuping Wen, Wenfeng Gong, Shengping Li, Yanji Jiang, Ji Zheng, Tianyi Zhu, Zihan Zhou, Xiaoyun Zeng, Ziliang Wang, Ji-Ao Wang, Rui Guo, Yuan Yang, Qingyi Wei, Gangqiao Zhou, Xiao-Qiang Qiu, Weizhong Tang, Mengyun Wang, Ruoxin Zhang

2026, 53(4): 643-654. doi: 10.1016/j.jgg.2025.11.003

Abstract (0) PDF (0)

Abstract:
Liver cancer ranks sixth in cancer incidence and third in cancer-related deaths worldwide. Hepatocellular carcinoma (HCC) is the primary histological subtype, and hepatitis B virus (HBV) carriers have a higher risk of HCC. Although several susceptibility loci for HCC have been identified in East Asian populations through genome-wide association studies (GWAS), the underlying biological mechanisms of this malignancy remain incompletely understood. Here, we conduct a two-stage GWAS including 2413 cases and 2794 HBV-positive controls from a high-incidence region in Southern China. The function of the susceptibility locus is investigated by bioinformatic and experimental approaches, supported by a xenograft model. We identify a 4p14 locus significantly associated with the risk of HCC (rs55718051, OR [95% CI] = 0.73 [0.67–0.80], P_meta = 9.14 × 10⁻¹¹), and 18q23 locus with borderline significance (rs12964643: OR [95% CI] = 0.75 [0.67–0.83], P_meta = 1.11 × 10⁻⁷). Functional experiments indicate the role of rs55718051 in FAM114A1 expression regulation, possibly through the interaction with FOXA1. Knockdown of FAM114A1 significantly promote the oncogenic phenotypes in liver cancer cells, suggesting its potential tumor suppressor role. Our findings expand the understanding of HCC susceptibility and suggest FAM114A1 as a potential suppressor in HBV-related HCC carcinogenesis.

Intrinsic NPRL2 and NPRL3 regulate the sensitivity of B-cell malignancies to CAR-T cell therapy

Fuxin Han, Yuting Lu, Yipeng Zhang, Xinran Ma, Chuan Tong, Jianshu Wei, Yelei Guo, Chun Liu, Zhiqiang Wu, Weidong Han, Yao Wang

2026, 53(4): 655-666. doi: 10.1016/j.jgg.2025.11.007

Abstract (0) PDF (0)

Abstract:
Although chimeric antigen receptor (CAR) T-cell therapy has markedly improved outcomes for many patients with B-cell malignancies, a subset experiences limited benefit due to primary or secondary resistance. Building on CRISPR/Cas9 genome-wide screening in malignant B-cells, we identify NPRL2 and NPRL3 as key regulators of tumor sensitivity to CAR-T cytotoxicity. This study aims to investigate the impact and mechanisms of tumor-intrinsic NPRL2 and NPRL3 on the efficacy of CAR-T cell therapy. In a tandem CD19/20 CAR-T clinical trial for relapsed/refractory (R/R) B-cell lymphoma (NCT03097770), high tumor NPRL2 or NPRL3 expression correlates with therapeutic resistance in patients. Consistently, in vitro experiments confirm that tumor cells overexpressing NPRL2/NPRL3 exhibit resistance to CAR-T-mediated cytolysis. Mechanistically, NPRL2/NPRL3 suppresses mTORC1 activity within tumor cells, negatively regulating the conjugation between tumor cells and CAR-T cells, consequently impairing CAR-T cell activation and cytotoxic function, ultimately facilitating immune escape. As therapeutic strategies, either genetic ablation of tumor-intrinsic NPRL2/NPRL3 or pharmacological activation of mTORC1 enhances CAR-T cell activation, cytotoxic degranulation, and tumor clearance both in vitro and in vivo. In conclusion, targeting tumor NPRL2/NPRL3 or directly activating mTOR represents a promising combinational strategy to potentiate CAR-T efficacy and overcome resistance in clinical practice.

hfCas12Max-mediated targeted integration at accessible chromatin regions with a goat-derived UCOE enhances stable recombinant lactoferrin expression

Zhenliang Zhu, Jing Han, Jianglin Zhao, Yangyi Jian, Yong Zhang, Yayi Liu, Peipei Bian, Zhenyu Wei, Xiaodan Ma, Rui Feng, Yuanpeng Gao, Jun Liu

2026, 53(4): 667-678. doi: 10.1016/j.jgg.2025.11.008

Abstract (0)

Abstract:
Stable transgene expression in the mammary gland is crucial for recombinant protein production in livestock, yet it is frequently hampered by transgene silencing and random integration. To address this, we profile chromatin accessibility in goat mammary epithelial cells (GMECs) using ATAC-seq and identify 15 highly accessible genomic regions. Three of these regions are confirmed to support stable transgene expression. Notably, we identify a goat-derived ubiquitous chromatin opening element (UCOE) in the SF3B1-COQ10B intergenic region, with a high GC content (65%) and CpG island enrichment. This UCOE improves hfCas12Max-mediated integration of large DNA fragments and maintains high-level expression of human lactoferrin (hLTF) in GMECs. Subsequently, we precisely integrate the UCOE-hLTF cassette into the highly accessible loci and generate a transgenic goat via somatic cell nuclear transfer, without detectable off-target effects. Our pipeline, which integrates chromatin accessibility profiling, UCOE discovery, and precision editing, demonstrates the role of CpG island-containing UCOEs in preventing transgene silencing. The study provides valuable tools for enhancing recombinant protein production, supports the breeding of dairy goats for milk with high lactoferrin content, and advances the understanding of the interactions between chromatin, regulatory elements, and transgenes in molecular breeding.

Maize Chlorotic Leaf Spot1 encodes a fumarylacetoacetate hydrolase essential for carbohydrate partitioning

Ruchang Ren, Sihang Zhao, Hong Jia, Hao Li, Lishuan Wu, Jinge Tian, Yifan Zhu, Junxiang Tang, Xiangyang Guo, Chenglong Wang, Feng Tian

2026, 53(4): 679-690. doi: 10.1016/j.jgg.2025.10.002

Abstract (41)

Abstract:
Carbohydrate partitioning from photosynthetic sources to non-photosynthetic sinks is essential for plant development and crop yield. Using a maize-teosinte BC₂S₃ population, we identify Chlorotic Leaf Spot1 (CLS1), a fumarylacetoacetate hydrolase (FAH) in the tyrosine degradation pathway that plays an essential role in carbohydrate partitioning in maize. CLS1 localizes to the plasma membrane, cytoplasm, and nucleus. Allelic tests and sequence analysis reveal that the teosinte parent CIMMYT8759 carries a weak allele of CLS1, likely due to rare amino acid substitutions at residues 175 and 355. Loss-of-function mutants of CLS1 develop chlorotic leaf spots accompanied by carbohydrate hyperaccumulation, reduced photosynthetic efficiency, chloroplast damage, and impaired transient starch conversion. Critically, cls1 mutants exhibit ectopic callose accumulation and aberrant plasmodesmata ultrastructure at the mesophyll-bundle sheath and bundle sheath-vascular parenchyma interfaces. This defect causes starch granule and soluble sugar accumulation in chlorotic leaf tissues, indicating a disruption of the symplastic transport pathway. Collectively, our results uncover an important role for FAH in plant development and identify CLS1 as a key regulator of symplastic carbohydrate partitioning.

ZmPRX38 is required for improving stalk strength and yield in maize

Xiaqing Wang, Tianyi Wang, Ruyang Zhang, Min Deng, Xuan Sun, Jinghuan Li, Dongmei Chen, Yanxin Zhao, Jidong Wang, Shuai Wang, Zhiyong Li, Ruibin Xu, Ronghuan Wang, Wei Song, Jiuran Zhao

2026, 53(4): 691-703. doi: 10.1016/j.jgg.2025.10.009

Abstract (0) PDF (2)

Abstract:
Stalk lodging is a major problem in maize production, usually causing significant yield losses due to weak stalk strength. Understanding the genetic basis of stalk strength is crucial for improving maize lodging resistance. In this study, we identify 31 quantitative trait loci (QTLs) related to maize stalk strength and clone ZmPRX38 (encoding peroxidase 38) responsible for a hotspot QTL region of stalk strength. ZmPRX38 is highly expressed in maize stalk during vegetative growth stage, and its protein is localized in the cell membrane, cytoplasm and apoplast. Knockout of ZmPRX38 decreases stalk strength and yield in maize, while overexpressing ZmPRX38 increases stalk strength and yield. ZmPRX38 in phenylpropanoid pathway is involved in the biosynthesis of guaiacyl lignin, p-hydroxy-phenyl lignin, and syringyl lignin. Additionally, we identify a favorable haplotype of ZmPRX38, which enhances stalk strength, containing three loci distributed in the 5′ untranslated region (UTR), exon 1, and 3′UTR of ZmPRX38, respectively. Although 91.46% of maize natural lines contain this favorable haplotype, most of the Huang-gai (HG) lines, a backbone maize germplasm, contain the unfavorable haplotypes. Therefore, targeted improvement of ZmPRX38 by editing unfavorable haplotypes may be an effective strategy for increasing maize stalk strength, thereby improving maize lodging resistance and yield.

Key divisions and cell specification during embryo pattern formation require SMU1-mediated splicing of CAK genes in Arabidopsis

Xiaoyi Huang, Yue Liu, Yajun Cai, Xiaogang Long, Emily Xu, Xiaoming Zhong, Jingyuan Zhang, Man Wang, Guoyong Xu, Peng Zhao, Kun Wang, Limin Pi, Arp Schnittger, Hongchun Yang

2026, 53(4): 704-718. doi: 10.1016/j.jgg.2025.10.008

Abstract (0)

Abstract:
Embryonic pattern formation and cell specification require precise cell division and cell cycle regulation. Splicing factors and the splicing of precursor mRNA (pre-mRNA) play significant roles in embryo development. However, how splicing factors control embryonic patterning via RNA splicing remains unclear. Here, we show that the mutation of SUPPRESSORS OF MEC-8 AND UNC-52 1 (SMU1), a conserved subunit of the spliceosomal B complex, causes compromised cell fate of the hypophysis and quiescent center (QC), failed embryonic root apical meristem (RAM) formation, as evidenced by altered WUSCHEL-RELATED HOMEOBOX 5 (WOX5) expression and perturbed auxin signaling. This results in smu1 embryo lethality. The splicing efficiency of three out of four CYCLIN-DEPENDENT KINASE ACTIVATOR (CAK) genes is decreased, leading to reduced protein levels in smu1 embryos. These CAK genes are required for hypophysis specification and embryonic RAM formation. SMU1 binds CAK transcripts in vitro and in vivo. Restoring the expression of either CAK gene partially rescues the defects in smu1 embryos, leading to the formation of QC-like cells, continued embryo development, and even the production of viable seeds. Our data suggest that SMU1 binds to CAK transcripts and promotes their splicing, enabling cell cycle progression to promote embryonic RAM formation.

Ribosomal protein bL31c interacts with translation elongation factor RAB8D to regulate chloroplast translation elongation and PSI-LHCI-LHCII assembly in Arabidopsis

Yukun Wang, Xiangsheng Ke, Shuaihao Chen, Jiabei Sun, Mi Zhou, La Bo, Hongkang Zhou, Qin Lu, Xin Hou

2026, 53(4): 719-731. doi: 10.1016/j.jgg.2025.11.006

Abstract (0) PDF (0)

Abstract:
Chloroplast translation systems have evolved specialized regulatory mechanisms distinct from those of their prokaryotic ancestors. However, critical gaps persist in understanding how these systems coordinate translation efficiency with photosynthetic apparatus assembly—a process central to plant development. Here, we identify Arabidopsis BACTERIAL LARGE RIBOSOMAL SUBUNIT PROTEIN 31 (bL31c) as a critical chloroplast ribosomal protein that interacts with the translation elongation factor RAB GTPASE HOMOLOG 8D (RAB8D) to ensure translation elongation efficiency. Knocking down bL31c disrupts chloroplast translation, causing preferential depletion of photosystem I (PSI) subunits, a functional imbalance between PSI and PSII, and paradoxical accumulation of the PSI-LHCI-LHCII supercomplex. Comparative analysis reveals evolutionary conservation of the bL31c-EF-Tu functional module in Cyanobacteria but not in Escherichia coli, demonstrating lineage-specific adaptation of translation surveillance mechanisms. Crucially, pharmacological inhibition of translation elongation in wild-type plants phenocopies the photosystem stoichiometry defects observed in bl31c mutants, establishing defective ribosome processivity as the primary driver of photosystem imbalance. Our findings uncover a plant-specific ribosomal checkpoint mechanism that dynamically coordinates protein synthesis with photosynthetic complex assembly, providing important insights into the evolutionary rewiring of organellar gene expression systems in eukaryotes.

Dual-target CRISPR-Cas12 diagnostics based on asymmetrically chemical-modified DNA probe

Xinge Wang, Yangcan Chen, Yanping Hu, Shengqiu Luo, Siqi Wang, Bangwei Mao, Changxian Peng, Chongjian Chen, Weiye Pan, Haiyan Yan, Jianyou Liao, Qi Zhou, Wei Li

2026, 53(4): 732-743. doi: 10.1016/j.jgg.2025.10.007

Abstract (47)

Abstract:
CRISPR-based nucleic acid detection technologies have revolutionized infectious disease detection and environmental monitoring by leveraging RNA–DNA complementarity to enable rapid, precise, and cost-effective detection of targets. However, achieving multitarget detection in one tube still presents challenges that necessitate further research. Here, we develop a nucleic acid detection module based on the CRISPR-Cas12i system. Importantly, we find that Cas12i and AapCas12b exhibit opposite trans-cleavage preferences for asymmetrically phosphorothioate-modified single-strand DNA probes, enabling the development of an effective dual-target nucleic acid detection platform by combining these two Cas12 nucleases in one tube. Moreover, this dual-target detection platform exhibits high specificity and sensitivity in genotyping the nucleic acid targets of human papillomavirus (HPV) 16 and HPV18, as well as Influenza A virus (FluA) and Respiratory syncytial virus. Notably, combined with loop-mediated isothermal amplification, this platform achieves high detection rates for clinical samples (18/18 FluA and 18/18 GAPDH internal reference detection rate). Taken together, these results can broaden the application of CRISPR-based Cas12 proteins for multi-target nucleic acid detection in one tube.

A universal and cost-efficient sample labeling approach for multiplexed single-cell RNA-seq based on recombinant HUH-endonuclease-agglutinin tagging

Quanyong Zhang, Maorong Li, Luemou Shen, Lujia Chen, Zhiheng Yuan, Xu Zhang, Hao Wang, Yang Yu, Fucheng Luo, Guangdun Peng, Jingjie Hu, Zhenmin Bao, Ning Song, Kai Chen

2026, 53(4): 744-757. doi: 10.1016/j.jgg.2025.10.004

Abstract (0)

Abstract:
Recent advances in single-cell transcriptomics have revolutionized our understanding of cellular diversity and tissue heterogeneity, providing unprecedented insights into biological and medical research. However, the high per-assay cost limits broader applications of this technology. Although sample labeling strategies enabling multiplexing have emerged, current methods suffer from either impractical complexity for barcoding or high cost for preparing the index labeling reagents. To address these challenges, here we present HUH-endonuclease-agglutinin tagging (HEATag), a universal cell membrane labeling approach that combines Duck circovirus HUH endonuclease (DCV) with wheat germ agglutinin (WGA) to efficiently tag cell membranes with indexed single-stranded DNA (ssDNA). The DCV domain enables rapid, sequence-specific conjugation of indexed ssDNA, while the WGA domain ensures robust labeling of fresh or fixed cells across diverse species. This method is compatible with both commercial platforms and custom systems, readily adaptable to various single-cell omics workflows. Therefore, HEATag provides a universal, cost-effective, and scalable solution for high-throughput single-cell studies, enhancing library preparation efficiency and minimizing batch effects for single-cell researchers.

Identification of a major locus Fhb.Er-3StS from Elymus repens conferring Fusarium head blight resistance in wheat

Fei Wang, Hanyu Wei, Hongjing Xu, Qianyi Guo, Wei Zhu, Lili Xu, Yiran Cheng, Yazhou Zhang, Yi Wang, Jian Zeng, Xing Fan, Yonghong Zhou, Dandan Wu, Yinghui Li, Houyang Kang

2026, 53(4): 758-761. doi: 10.1016/j.jgg.2025.11.013

Abstract (0)

Abstract:

CellReasoner: a reasoning-enhanced large language model for cell type annotation

Guangshuo Cao, Yi Shen, Lingyu Zhao, Jianghong Wu, Haoyu Chao, Ming Chen, Dijun Chen

2026, 53(4): 762-765. doi: 10.1016/j.jgg.2025.11.012

Abstract (0)

Abstract:

2026 Vol. 53, No. 4