Journal of Genetics and Genomics最新文献

Hybridization reshapes maize phenotypic plasticity through coordinated changes in environmental responses and genetic architecture.

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-11-02 DOI: 10.1016/j.jgg.2026.10.016

Yilan Cao, Xiangjian Gou, Zhenwei Zhang, Haitao Li, He Pei, Shuang Zhang, Lingju Zeng, Haoyan Yang, Xianlong Song, Xiaoyan Qian, Nannan Liu, Yingjie Xiao, Jianbing Yan, Tingting Guo

{"title":"Hybridization reshapes maize phenotypic plasticity through coordinated changes in environmental responses and genetic architecture.","authors":"Yilan Cao, Xiangjian Gou, Zhenwei Zhang, Haitao Li, He Pei, Shuang Zhang, Lingju Zeng, Haoyan Yang, Xianlong Song, Xiaoyan Qian, Nannan Liu, Yingjie Xiao, Jianbing Yan, Tingting Guo","doi":"10.1016/j.jgg.2026.10.016","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.016","url":null,"abstract":"Phenotypic plasticity is central to crop adaptation under climate variability, yet how hybridization reshapes it remains unclear. Here, we integrate multi-environment phenotypes, environmental variables, and genomic data from 456 maize inbred lines and 912 corresponding hybrids evaluated across 11 environments to dissect the environmental and genetic bases of plasticity for flowering time, plant height, and ear weight. Reaction-norm analyses reveal two- to three-fold greater plasticity variation in inbreds than hybrids, indicating more uniform plastic responses in hybrids. Environmental association analyses demonstrate that inbreds and hybrids respond to the same environmental factors with different magnitudes or even opposite directions (e.g., correlations between diurnal temperature range and flowering time ranged from -0.73 to -0.14 in inbreds but 0.22 to 0.46 in hybrids). Genome-wide association analyses identify distinct parental loci for plasticity, with more loci and larger effects in hybrids. Functional validation shows that ZmBAF60_13, a chromatin-remodeling gene found only in the inbred panel, negatively regulates flowering-time plasticity. Integrating multiple environmental indices improves phenotype prediction accuracy by up to 16% over single-index models. Together, this study reveals that hybrids exhibit reduced plasticity variation and differ from inbreds in environmental responses and genetic associations, providing a framework for predicting crop performance under climate variability.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149327594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activating death receptor 5 exposes a cancer cell vulnerability to natural killer and T cell attack.

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-11-02 DOI: 10.1016/j.jgg.2026.10.015

Zhen Chen, Gabriele Casagrande Raffi, Ziji Zhao, Chaopin Yang, Jian Chen, Xuezhao Feng, Yanxing Chen, Marit Steur, Pietro Morandi, Cor Lieftink, Siyi Lu, Huamei Xie, Haoran Zhong, Jing Wang, Lisa Willemsen, Hugo Horlings, Roderick Beijersbergen, Krijn K Dijkstra, Song Gao, Ruidong Xue, Rene Bernards, Liqin Wang

{"title":"Activating death receptor 5 exposes a cancer cell vulnerability to natural killer and T cell attack.","authors":"Zhen Chen, Gabriele Casagrande Raffi, Ziji Zhao, Chaopin Yang, Jian Chen, Xuezhao Feng, Yanxing Chen, Marit Steur, Pietro Morandi, Cor Lieftink, Siyi Lu, Huamei Xie, Haoran Zhong, Jing Wang, Lisa Willemsen, Hugo Horlings, Roderick Beijersbergen, Krijn K Dijkstra, Song Gao, Ruidong Xue, Rene Bernards, Liqin Wang","doi":"10.1016/j.jgg.2026.10.015","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.015","url":null,"abstract":"Immunotherapy has revolutionized cancer care, yet resistance frequently undermines its efficacy. Although tumor-intrinsic resistance pathways have been mapped, how immune pressure regulates death-receptor vulnerability and anti-apoptotic buffering remains less defined. Using genome-wide CRISPR-Cas9 screening in cancer cells co-cultured with natural killer (NK) cells, we identify CFLAR, encoding cFLIP, as a dominant suppressor of death-receptor signaling that impairs NK- and T-cell cytotoxicity. CFLAR depletion sensitizes cancer cells to NK- and T-cell attack in vitro and in vivo. Single-cell and spatial transcriptomic analyses link high CFLAR expression to reduced lymphocyte infiltration and poorer responses to immune checkpoint blockade. Mechanistically, immune effector cell-induced inflammation increases CFLAR and death receptor 5 (DR5) expression in association with p38-MAPK signaling, balancing survival and death under immune pressure. The DR5 agonist conatumumab enhances lymphocyte-mediated killing and improves responses to cellular therapies, checkpoint blockade, and chemo-immunotherapy. Combining DR5 agonism with NKG2A blockade co-activates NK- and T-cell responses and overcomes anti-PD-1 resistance in MHC-I-deficient tumors. These findings identify the DR5-cFLIP axis as an immune-pressure-associated, pharmacologically targetable vulnerability and support rational combinations of DR5 agonists with multiple immunotherapies for refractory cancers.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149327593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactylation at the crossroads: a metabolic-epigenetic-immune integrator in intestinal homeostasis and disease. 十字路口的乳酸化：肠道内稳态和疾病中的代谢-表观遗传-免疫整合物。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-27 DOI: 10.1016/j.jgg.2026.10.010

Jingli Ao, Yingwei Li, Xinbei Lin, Bufu Tang, Lianxiang Luo

{"title":"Lactylation at the crossroads: a metabolic-epigenetic-immune integrator in intestinal homeostasis and disease.","authors":"Jingli Ao, Yingwei Li, Xinbei Lin, Bufu Tang, Lianxiang Luo","doi":"10.1016/j.jgg.2026.10.010","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.010","url":null,"abstract":"Lysine lactylation (Kla) is a metabolite-sensitive post-translational modification implicated in DNA repair, tumorigenesis, chemoresistance, and innate immunity. Recent studies also implicate Kla in intestinal disorders. This review synthesizes current evidence on protein lactylation in intestinal inflammation, inflammatory bowel disease, colorectal cancer, irritable bowel syndrome, intestinal fibrosis, radiation-induced injury, and enteric infection. We distinguish lactate-mediated receptor signaling and metabolic effects from covalent Kla, compare evidence across cell types and disease stages, and assess preclinical strategies targeting the lactate-lactylation axis. We also discuss microbiota-host metabolic crosstalk and mucus-penetrating nanodelivery, including the cross-border emulsification effect, an oil-in-water double-emulsion concept that describes traversal of the mucus barrier rather than a biochemical form of lactylation. Collectively, the available evidence supports a metabolism-epigenetics-immunity framework for gut pathophysiology, while highlighting unresolved questions concerning stereochemistry, site specificity, causality, safety, and prospective clinical validation.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149290048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A yak pangenome reveals whole-genome structural variations underlying domestication and introgression from cattle. 牦牛全基因组揭示了驯化和从牛遗传渗入的全基因组结构变异。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-27 DOI: 10.1016/j.jgg.2026.10.012

Yi Liu, Yuan Xu, Jiawei Lu, Xian Guo, Xingdong Wang, Niyazbekova Zhannur, Gaoyue Liu, Zhengrong Yuan, Yu Jiang, Yi Ma

引用次数: 0

Protein palmitoylation in disease: decoding its crosstalk with ubiquitination and phosphorylation for pathogenic mechanisms and targeted therapeutics. 疾病中的蛋白棕榈酰化：解码泛素化和磷酸化的串音，用于致病机制和靶向治疗。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-26 DOI: 10.1016/j.jgg.2026.10.014

Sainan Li, Huanjin Suo, Renqiang Hao, Ruohan Wu, Yinming Liang, Eryan Kong, Liu Cao, Binhui Zhou

{"title":"Protein palmitoylation in disease: decoding its crosstalk with ubiquitination and phosphorylation for pathogenic mechanisms and targeted therapeutics.","authors":"Sainan Li, Huanjin Suo, Renqiang Hao, Ruohan Wu, Yinming Liang, Eryan Kong, Liu Cao, Binhui Zhou","doi":"10.1016/j.jgg.2026.10.014","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.014","url":null,"abstract":"Protein S-palmitoylation is a reversible lipid modification that governs protein stability, trafficking, and signaling. Rather than an isolated tag, it acts as a spatiotemporal routing signal within an integrated post-translational modification (PTM) network, engaging in three defined crosstalk modes with ubiquitination and phosphorylation: synergistic, antagonistic, and cascading. Although crosstalk with acetylation and myristoylation exists, this review focuses on the ubiquitination- and phosphorylation-centered networks most directly linked to palmitoylation in disease. The same palmitoylation event can stabilize or destabilize substrates, or activate or silence signaling, depending on the specific Zinc finger DHHC domain-containing protein (ZDHHC) isoform, subcellular location, local enzyme availability, and metabolic state. We further introduce the \"PTM context signature\", a four-variable predictive framework for disease-specific crosstalk outcomes. By dissecting palmitoylation-centered crosstalk through a disease-oriented lens, we examine how its dysregulation drives oncogenesis, inflammation, metabolic disorders, and neurodegeneration. We then translate these mechanistic principles into a network-centric therapeutic framework, evaluating ZDHHC-directed modulators, peptide-based interface disruptors, and crosstalk-informed combinations that target context-specific nodes and anticipate therapy resistance. Viewing palmitoylation as an integrated component of the cellular PTM network, rather than as an isolated lipid tag, provides a framework for understanding disease pathogenesis and for targeting PTM networks rather than single modifications.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149277375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

From loci to mechanisms: wheat autoimmunity as a window into plant immune activation. 从基因座到机制：小麦自身免疫作为植物免疫激活的窗口。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-26 DOI: 10.1016/j.jgg.2026.10.013

Wenling Li, Miao He, Fei Xiong, Qiuhong Wu, Haiyan Jia, Zhiyong Liu

{"title":"From loci to mechanisms: wheat autoimmunity as a window into plant immune activation.","authors":"Wenling Li, Miao He, Fei Xiong, Qiuhong Wu, Haiyan Jia, Zhiyong Liu","doi":"10.1016/j.jgg.2026.10.013","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.013","url":null,"abstract":"Wheat (Triticum aestivum L.) is a major staple crop, and developing broad-spectrum resistance to multiple fungal pathogens is essential for sustainable production. Wheat autoimmunity (WAI) mutants represent genetic resources that spontaneously activate immune responses under non-stress conditions, exhibiting lesion-mimic or leaf-tip necrosis phenotypes and enhanced resistance to multiple foliar diseases, including powdery mildew and rusts. Increasing evidence indicates that WAI arises from dysregulation of immune homeostasis across multiple regulatory levels, involving receptor activation, cellular homeostasis, and membrane transport processes, ultimately converging on evolutionarily conserved defense outputs such as reactive oxygen species (ROS) accumulation, activation of defense-related genes, ion fluxes, and programmed cell death (PCD). Recent advances have identified key WAI-associated loci, including nucleotide-binding and leucine-rich-repeat receptors (NLRs), membrane proteins, regulatory components, and transporters, revealing mechanistically distinct pathways underlying constitutive immunity and its trade-off with growth. This review summarizes recent progress in the genetics and molecular mechanisms of WAI, critically assesses its roles in broad-spectrum, multi-disease resistance, and discusses strategies to minimize the growth and fitness costs. Furthermore, we propose that structure-guided allele optimization combined with spatiotemporal regulation of gene expression holds promise for the rational engineering of WAI alleles that confer durable disease resistance while minimizing associated fitness costs.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149277385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

mRNA alternative splicing dysregulation in oocytes causes premature ovarian failure. 卵母细胞mRNA选择性剪接失调导致卵巢早衰。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-24 DOI: 10.1016/j.jgg.2026.10.011

Wei Yue, Yi-Xiao Li, Di Gao, Rui-Ying Yuan, Hong-Yong Zhang, Shu-Chen Liu, Xu-Feng Li, Zheng-Hui Zhao, Qing-Yuan Sun, Tie-Gang Meng

{"title":"mRNA alternative splicing dysregulation in oocytes causes premature ovarian failure.","authors":"Wei Yue, Yi-Xiao Li, Di Gao, Rui-Ying Yuan, Hong-Yong Zhang, Shu-Chen Liu, Xu-Feng Li, Zheng-Hui Zhao, Qing-Yuan Sun, Tie-Gang Meng","doi":"10.1016/j.jgg.2026.10.011","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.011","url":null,"abstract":"Primordial follicle survival determines female reproductive lifespan, yet the post-transcriptional mechanisms governing this process remain incompletely understood. Here, we show that the splicing regulator SRSF2 is required for maintaining the ovarian follicle reserve through the regulation of RNA processing in oocytes. Oocyte-specific ablation of Srsf2 using Gdf9-Cre causes complete female infertility, progressive follicular depletion, and increased follicular apoptosis. Linear amplification of complementary DNA ends and sequencing (LACE-seq) identifies 1609 SRSF2-bound transcripts enriched in RNA-regulatory and cellular homeostasis-related processes. Subsequent RNA-seq analysis reveals broad transcriptomic and alternative-splicing dysregulation after Srsf2 loss, including prominent exon 7 skipping of the oocyte-specific transcription factor Nobox and a marked reduction in full-length NOBOX protein. Supplementation with correctly spliced Nobox mRNA partially rescues follicular developmental defects in vitro, supporting Nobox as a functionally important downstream target rather than the sole mediator of the Srsf2-deficient phenotype. Together, these findings identify SRSF2-dependent RNA processing as an important regulator of oocyte and follicle homeostasis and suggest that disruption of SRSF2-regulated splicing may contribute to ovarian insufficiency.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149277323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ancient-modern genomics reveals the geographic origins of the historical Huangqi specimen from the Qing Imperial Pharmacy. 古今基因组学揭示了清朝皇家药房历史黄芪标本的地理起源。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-21 DOI: 10.1016/j.jgg.2026.10.009

Xiaojing Han, Minzhen Yin, Fengyuan Li, Zhengyang Yang, Yuanyang Cai, Yucheng Wang, Huasheng Peng, Luqi Huang

引用次数: 0

LSD1 exerts crucial functions to drive the progression of meiotic prophase I during spermatogenesis. 在精子发生过程中，LSD1在驱动减数分裂前期I的进程中发挥着至关重要的作用。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-19 DOI: 10.1016/j.jgg.2026.10.008

Tianhua Zhu, Shaogang Qin, Yingying Dong, Hong Li, Qingfeng Yang, Chenmin Zhou, Yibing Bao, Zijian Zhu, Fengchao Wang, Guoliang Xia, Bo Zhou, Chao Wang, Zhengpin Wang

{"title":"LSD1 exerts crucial functions to drive the progression of meiotic prophase I during spermatogenesis.","authors":"Tianhua Zhu, Shaogang Qin, Yingying Dong, Hong Li, Qingfeng Yang, Chenmin Zhou, Yibing Bao, Zijian Zhu, Fengchao Wang, Guoliang Xia, Bo Zhou, Chao Wang, Zhengpin Wang","doi":"10.1016/j.jgg.2026.10.008","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.008","url":null,"abstract":"Epigenetic modifications are critical determinants governing the proper initiation and progression of gametogenesis. Accumulating evidence has indicated that epigenetic dysregulation underlies the pathogenesis of infertility. However, detailed information on the individual powerful roles of these epigenetic enzymes in facilitating programmed meiosis remains elusive. This study indicates that lysine-specific demethylase 1 (LSD1) plays critical roles during meiotic prophase I in mouse spermatogenesis. Germ cell-specific deletion of the Lsd1 gene in male mice caused meiotic arrest at the pachytene stage, ultimately leading to infertility. In primary spermatocytes of Lsd1-deficient mice, compromised homologous chromosome synapsis and DNA double-strand break repair activated the DNA damage checkpoint pathway, triggering spermatocyte apoptosis. Mechanistically, LSD1 directly binds to the promoters of meiotic genes, including Prdm9 and Rpa2, to regulate their expression during meiosis. PRDM9 and RPA2 are upregulated upon LSD1 loss and are essential for homologous recombination and DNA double-strand break repair. The promoters of Prdm9 and Rpa2 are also occupied by H3K4me2, whose levels increase upon LSD1 loss. Collectively, this study highlights the crucial role of LSD1 in orchestrating meiotic genes, possibly through its demethylase activity during spermatogenesis, and may help explain the pathology of non-obstructive azoospermia in humans.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DNAJC17 regulates RNA splicing in auditory hair cells and is required for hearing. DNAJC17调节听觉毛细胞中的RNA剪接，是听力所必需的。

IF 7.9 2区生物学

Journal of Genetics and Genomics Pub Date : 2026-10-13 DOI: 10.1016/j.jgg.2026.10.007

Luping Zhang, Ziyang Wang, Wenya Fan, Yiliang Huang, Chenxuan Yong, Yuecen Sun, Qingyue Yuan, Guang-Jie Zhu, Ao Li, Tao Yang, Qing Liu, Guoqiang Wan

{"title":"DNAJC17 regulates RNA splicing in auditory hair cells and is required for hearing.","authors":"Luping Zhang, Ziyang Wang, Wenya Fan, Yiliang Huang, Chenxuan Yong, Yuecen Sun, Qingyue Yuan, Guang-Jie Zhu, Ao Li, Tao Yang, Qing Liu, Guoqiang Wan","doi":"10.1016/j.jgg.2026.10.007","DOIUrl":"https://doi.org/10.1016/j.jgg.2026.10.007","url":null,"abstract":"RNA splicing is essential for gene regulation, but its role in maintaining cochlear hair cell function remains incompletely understood. Here, we identify a heterozygous missense variant (c.401A>C, p.E134A) in DNAJC17, which encodes a spliceosome-associated protein, that segregates with adult-onset progressive hearing loss in a multigenerational family. Hair cell-specific deletion of Dnajc17 in mice results in profound deafness with progressive hair cell degeneration, establishing its essential role in cochlear maintenance. Hair cells lacking DNAJC17 exhibit marked stereocilia disorganization accompanied by widespread alternative splicing defects in the cochlea. Notably, the dual-specificity protein kinase Clk1 that regulates pre-mRNA splicing shows altered exon inclusion, consistent with disruption of splicing control networks. In addition, Dnajc17 p.E134A knock-in mice develop adult-onset progressive hearing loss with stereocilia and mitochondrial abnormalities but preserve hair cell survival, recapitulating the human phenotype. Together, these findings identify DNAJC17 as a causative gene for autosomal dominant hearing loss and identify RNA splicing regulation as a key mechanism required for long-term maintenance of cochlear hair cell integrity.","PeriodicalId":54825,"journal":{"name":"Journal of Genetics and Genomics","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0