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Transposon–host arms race: a saga of genome evolution

Trends in Genetics 2025年第5期41卷 369-389页

作者： Iwasaki, Yuka W. Shoji, Keisuke Nakagwa, Shinichi Miyoshi, Tomoichiro Tomari, Yukihide Laboratory for Functional Non-coding Genomics RIKEN Center for Integrative Medical Sciences 1-7-22 Suehiro-cho Tsurumi-ku Kanagawa Yokohama 230-0045 Japan of Bio-Applications and Systems Engineering Tokyo University of Agriculture and Technology Tokyo Koganei-shi 184-8588 Japan Laboratory of RNA Function Institute for Quantitative Biosciences The University of Tokyo 1-1-1 Yayoi Tokyo Bunkyo-ku 113-0032 Japan RNA Biology Laboratory Faculty of Pharmaceutical Sciences Hokkaido University Kita 12-jo Nishi 6-chome Kita-ku Sapporo 060-0812 Japan Laboratory for Retrotransposon Dynamics RIKEN Center for Integrative Medical Sciences 1-7-22 Suehiro-cho Tsurumi-ku Kanagawa Yokohama 230-0045 Japan Department of Computational Biology and Medical Sciences of Frontier Sciences The University of Tokyo Tokyo Bunkyo-ku 113-0032 Japan

Once considered ‘junk DNA,’ transposons or transposable elements (TEs) are now recognized as key drivers of genome evolution, contributing to genetic diversity, gene regulation, and species diversification. However, their ability to move within the genome poses a potential threat to genome integrity, promoting the evolution of robust host defense systems such as Krüppel-associated box (KRAB) domain-containing zinc finger proteins (KRAB-ZFPs), the human silencing hub (HUSH) complex, 4.5SH rnas, and PIWI-interacting rnas (pirnas). This ongoing evolutionary arms race between TEs and host defenses continuously reshapes genome architecture and function. This review outlines various host defense mechanisms and explores the dynamic coevolution of TEs and host defenses in animals, highlighting how the defense mechanisms not only safeguard the host genomes but also drive genetic innovation through the arms race. © 2025 Elsevier Ltd

关键词： evolutionary arms race genetic conflicts genome evolution host defense mechanisms transposable elements (TEs)

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Rosaceae phylogenomic studies provide insights into the evolution of new genes

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Horticultural Plant Journal 2025年第1期11卷 389-405页

作者： Lan Jiang Xiaoxu Li Kun Lyu Han Wang Zhiyuan Li Wang Qi Lin Zhang Yunpeng Cao Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation(Wannan Medical College) Central LaboratoryYijishan Hospital of Wannan Medical CollegeWuhuAnhui 241000China Beijing Life Science Academy Beijing 102209China CAS Key Laboratory of Plant Germplasm Enhancement and Specialty Agriculture Wuhan Botanical GardenChinese Academy of SciencesWuhanHubei 430074China Center of Economic Botany Core Botanical GardensChinese Academy of SciencesWuhanHubei 430074China Key Laboratory for Tobacco Gene Resources Tobacco Research InstituteChinese Academy of Agricultural SciencesQingdaoShangdong 266000China school of Life Sciences Anhui Agricultural UniversityHefeiAnhui 230036China School of Basic Medical Sciences Hubei University of Chinese MedicineWuhanHubei 430065China

Rosa banksiae,known as Lady Banks'rose,is a perennial ornamental crop and a versatile herb in traditional Chinese *** the lack of genomic resources,we assembled a Hi Fi and Nanopore sequencing-derived 458.58 Mb gap-free telomere-to-telomere high-quality *** genome with a scaffold N50=63.90 *** genome of *** exhibited no lineage-specific whole-genome duplication compared with other *** phylogenomic analysis of 13 Rosaceae and Arabidopsis through a comparative genomics study showed that numerous gene families were lineage-specific both before and after the diversification of *** of these genes are candidates for new genes that have evolved from parental genes through fusion *** genes are divided into three types:Type-I and Type-II genes contain two parental genes that are generated by duplication,distributed in the same and different regions of the genome,respectively;and Type-III can only be detected in one parental ***,Type-I genes are found to have more relaxed selection pressure and lower Ks values than Type-II,indicating that these newly evolved Type-I genes may play important roles in driving phenotypic *** analysis exhibited that newly formed fusion genes can regulate the phenotype traits of plant growth and development,suggesting the functional significance of these *** study identifies new fusion genes that could be responsible for phenotype evolution and provides information on the evolutionary history of recently diverged species in the Rosa *** data represents the major progress in understanding the new fusion genes evolution pattern of Rosaceae and provides an invaluable resource for phylogenomic studies in plants.

关键词： Rosa banksiae Gap-free genome Rosaceae Phenotype Evolutionary patterns

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Ginsenoside Rg5 alleviates radiation-induced acute lung vascular endothelium injury by reducing mitochondrial apoptosis via Sirt1

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Journal of Ginseng Research 2025年第3期49卷 260-270页

作者： Li, Churong Zhao, Biao Xiong, Jing Li, Linjie Pang, Dalong Unger, Keith Jung, Mira Lyu, Jiahua Kuang, Hao Liang, Long Li, Tao Chen, Long Bai, Hansong Radiotherapy Center Radiation Oncology Key Laboratory of Sichuan Province Sichuan Clinical Research Center for Cancer Sichuan Cancer Hospital & Institute Sichuan Cancer Center University of Electronic Science and Technology of China Chengdu China Non-Coding RNA and Drug Discovery Key Laboratory of Sichuan Province School of Basic Medical Sciences Chengdu Medical College Chengdu China Department of Integrative Chinese and Western Medicine Sichuan Cancer Hospital & Institute Sichuan Cancer Center Affiliated Cancer Hospital of the University of Electronic Science and Technology of China Chengdu China Department of Immunology School of Basic Medical Sciences Chengdu Medical College Chengdu China Department of Radiation Medicine Lombardi Comprehensive Cancer Center Georgetown University Medical Center Washington DC United States Department of Oncology The Affiliated Hospital of Southwest Medical University Luzhou China School of Medicine University of Electronic Science and Technology of China Chengdu China

Background: Ginsenoside Rg5 possesses potent anti-oxidative, anti-inflammatory, and cytoprotective properties. This study explored the protective effects of ginsenoside Rg5 on radiation-induced pulmonary microvascular endothelial cells (PMECs) injury and the associated molecular mechanisms. Materials and methods: C57BL/6 mice were used for in vivo studies and primary human PMECs (PPMECs) were utilized as in vitro models. Mice with or without ginsenoside Rg5 pretreatment were irradiated by varying doses. Lung tissues were analyzed for histopathological changes and the expression of endothelial markers. In vitro, PPMECs were irradiated with or without ginsenoside Rg5 pretreatment and analyzed for apoptosis, oxidative stress, mitochondrial function, and endothelial barrier integrity. Results: Ginsenoside Rg5 pretreatment attenuated radiation-induced acute lung damage, preserved endothelial cell junction integrity, and maintained endothelial barrier function in vivo. In vitro, ginsenoside Rg5 significantly reduced IR-induced oxidative stress, apoptosis, and mitochondrial dysfunction in PPMECs. Ginsenoside Rg5 suppressed radiation-induced Mfn2 acetylation and proteasomal degradation via Sirt1-mediated deacetylation, thereby preserving mitochondrial dynamics and integrity. The protective effects of ginsenoside Rg5 on the integrity of mitochondrial and endothelial tight junction proteins and barrier function were also Sirt1-dependent. Conclusions: Ginsenoside Rg5 exerts a protective effect against radiation-induced endothelial injury by modulating mitochondrial dynamics and function, as well as maintaining endothelial barrier integrity, in a Sirt1-dependent manner. © 2025

关键词： Endothelial cell injury Ginsenoside Rg5 Mitochondrial dynamics Radiation Sirt1

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Carnitine palmitoyltransferase 1C promotes EMT-associated cisplatin resistance in non-small cell lung cancer cells

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Cancer Biology & Medicine 2025年第1期22卷 48-66页

作者： Renjie Chen Jiahui Wang Shuoyu Huang Xuefeng Hu Xinran He Tiange Zhang Yunhan Hu Huijun Wei Sihui Nian Yushu Huang Zhihao Wu Research Laboratory of Tumor Microenvironment Wannan Medical CollegeWuhu 241001China School of Laboratory Medicine Wannan Medical CollegeWuhu 241001China School of Anesthesiology Wannan Medical CollegeWuhu 241001China School of Medical Imageology Wannan Medical CollegeWuhu 241001China School of Clinical Medicine Wannan Medical CollegeWuhu 241001China Anhui Province Key Laboratory of Active Biological Macro-molecules Research Wannan Medical CollegeWuhu 241001China Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui Wannan Medical CollegeWuhu 241001China School of Pharmacy Wannan Medical CollegeWuhu 241001China Anhui Province Key Laboratory of Non-coding RNA Basic and Clinical Transformation Wannan Medical CollegeWuhu 241001China Anhui Provincial Engineering Research Center for Dental Materials and Application Wannan Medical CollegeWuhu 241001China

Objective:Lung cancer is the most common cause of cancer-related deaths ***-based chemotherapy is one of the main treatment options for patients with non-small cell lung cancer(NSCLC)but the effectiveness of chemotherapy is encumbered by drug ***,understanding the molecular mechanisms underlying chemotherapy resistance is crucial in improving treatment outcomes and ***:The cell viability assay and apoptosis were used to analyze *** blot analysis and wound healing testing were used to evaluate the epithelial-to-mesenchymal transition(EMT).Immunoprecipitation was used for analysis of protein *** activity was determined using the luciferase reporter *** staining was used to determine reactive oxygen species *** expression patterns of EMT markers and carnitine palmitoyltransferase 1C(CPT1C)were determined by Western blot ***:CPT1C,which was shown to be highly expressed in lung cancer,is associated with cisplatin resistance in NSCLC ***1C depletion increased NSCLC cell sensitivity to cisplatin,while overexpression of CPT1C increased NSCLC cell resistance to *** of EMT mediated CPT1C-induced cisplatin *** expression of Snail reversed the increase in cisplatin sensitivity triggered by CPT1C ***,CPT1C was shown to be regulated at the post-translational level and an E3-ubiquitin ligase,NEDD4L,was shown to be a major regulator of CPT1C stability and ***:These data provide evidence for the first time that the lipid metabolism enzyme,CPT1C,mediates resistance to ***,the use of combination therapy with a CPT1C inhibitor may be a promising new avenue in lung cancer treatment.

关键词： CPT1C chemoresistance EMT NEDD4L NSCLC

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Inhibition of KDM6B prevents osteoarthritis by blocking growth plate-like H3K27me3 loss in bivalent genes

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Science China Life Sciences 2025年第5期68卷 1423-1436页

作者： Hao Du Yao Zhang Xi Yu Xuanhe You Diwei Wu Ze Du Yongrui Cai Zhenyu Luo Hanpeng Lu Zhixin Liao Bi-Sen Ding Ya Zhao Yan Wang Ke Xiao Fan Yang Fangji Gan Ning Ning Jiancheng Zeng Peiliang Shi Zongke Zhou Shishu Huang Department of Orthopedic Surgery and Orthopedic Research Institute West China HospitalSichuan University Rehabilitation Medicine Center West China HospitalSichuan University Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE State Key Laboratory of BiotherapyWest China Second University HospitalSichuan University Institute of Translational Medicine Medical CollegeYangzhou University Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research College of Animal Science and Technology Sichuan Agricultural University Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province Sichuan Agricultural University Department of Lower Limb Surgery of Sichuan Province Orthopedic Hospital Central Laboratory of Sichuan Province Orthopedic Hospital Brain Cognition and Brain Disease Institute (BCBDI) Shenzhen Institute of Advanced TechnologyChinese Academy of Sciences (CAS)Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions School of Mechanical Engineering Sichuan University Gem Pharmatech (Chengdu) Co. Ltd.

Osteoarthritis(OA) is the most prevalent joint disorder occurring with articular cartilage degradation. It includes a switch from an articular to a growth plate chondrocyte phenotype. Here, we investigated the histone modification profiles and found significant H3K27me3 loss in OA, which led to disease-associated gene expression. Surprisingly, these genes were occupied by both H3K27me3 and H3K4me3 in normal chondrocytes, showing a poised bivalent state. Furthermore, we observed the derepression of similar bivalent genes in growth plate chondrocytes. Finally, a KDM6B inhibitor GSK-J4 prevented the H3K27me3 loss and cartilage damage in the rat OA model. Our results reveal an inherited bivalent epigenetic signature on developmental genes that makes articular chondrocytes prone to hypertrophy and contributes to a promising epigenetic therapy for OA.

关键词： osteoarthritis histone modifications H3K27me3 bivalency growth plate

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Improved immunocompatibility of active targeting liposomes by attenuating nucleophilic attack of cyclic RGD peptides on complement 3

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Biomaterials 2025年 321卷 123350-123350页

作者： Meng, Nana Lu, Jiasheng Zhou, Jianfen Yang, Shengmin Zhang, Chen Jia, Ruiyi Ding, Yuan Bao, Yanning Wang, Jun Ma, Xiaopei Chen, Ruohan Jiang, Zhixuan Xie, Cao Lu, Linwei Lu, Weiyue Department of Pharmaceutics School of Pharmacy Fudan University & National Key Laboratory of Advanced Drug Formulations for Overcoming Delivery Barriers Shanghai201203 China Department of Integrative Medicine Huashan Hospital Fudan University Shanghai200040 China Institutes of Integrative Medicine Fudan University Shanghai200040 China Shanghai Engineering Technology Research Center for Pharmaceutical Intelligent Equipment and Shanghai Frontiers Science Center for Druggability of Cardiovascular Non-coding RNA Institute for Frontier Medical Technology Shanghai University of Engineering Science Shanghai201620 China

One of the challenges for the clinical translation of active targeting nanomedicines is the adverse interactions between targeting ligands and blood components. Herein, a novel regularity, which reveals the interactions between cyclic RGD (Arg-Gly-Asp) peptide-modified liposomes and complement components in blood, is reported. As the nucleophilicity of arginine guanidine group within the cyclic RGD-like peptide increases, targeting liposomes potentiate complement cascade via the amplification loop of complement 3 (C3), ultimately leading to accelerated blood clearance, increased deposition in the reticuloendothelial system (RES) organs, enhanced immune responses, and potential side effects. By appropriately reducing the nucleophilicity of guanidine group, cyclic R2 peptide is designed for modification of liposomes to target integrin αvβ3. Compared to the widely used targeting molecule c(RGDyK), R2 eliminates the negative effects of C3 opsonization and specific antibody production, significantly improves the in vivo immunocompatibility of targeting liposomes, and demonstrates superior anti-tumor efficacy in mouse models of orthotopic breast cancer and glioma. Thus, the proposed regularity of interactions between guanidine nucleophilicity and C3, along with the successful application of the low complement activation capacity targeting ligand R2, provides new insights for addressing challenges related to complement activation in the clinical translation of active targeting nanomedicines. © 2025 Elsevier Ltd

关键词： Ligands

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Corrigendum to Exosomal mirna confers chemo resistance via targeting Cav1/p-gp/M2-type macrophage axis in ovarian cancer

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EBioMedicine 2025年 111卷 105486页

作者： Pinar Kanlikilicer Recep Bayraktar Merve Denizli Mohammed H Rashed Cristina Ivan Burcu Aslan Rahul Mitra Kubra Karagoz Emine Bayraktar Xinna Zhang Cristian Rodriguez-Aguayo Amr Ahmed El-Arabey Nermin Kahraman Seyda Baydogan Ozgur Ozkayar Michael L Gatza Bulent Ozpolat George A Calin Anil K Sood Gabriel Lopez-Berestein Department of Experimental Therapeutics The University of Texas MD Anderson Cancer Center Houston TX USA Center for RNA Interference and Non-Coding RNA The University of Texas MD Anderson Cancer Center Houston TX USA. Department of Experimental Therapeutics The University of Texas MD Anderson Cancer Center Houston TX USA. Center for RNA Interference and Non-Coding RNA The University of Texas MD Anderson Cancer Center Houston TX USA Department of Gynecologic Oncology and Reproductive Medicine The University of Texas MD Anderson Cancer Center Houston TX USA. Rutgers Cancer Institute of New Jersey New Brunswick NJ USA. Hacettepe University Ankara Turkey. Department of Cancer Biology The University of Texas MD Anderson Cancer Center Houston TX USA. Department of Cancer Biology The University of Texas MD Anderson Cancer Center Houston TX USA Department of Cancer Biology The University of Texas MD Anderson Cancer Center Houston TX USA. Electronic address: glopez@***.

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Calcium-mediated oxidative stress: a common mechanism in tight junction disruption by different types of cellular stress

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BIOCHEMICAL JOUrnaL 2017年第5期474卷 731-749页

作者： Gangwar, Ruchika Meena, Avtar S. Shukla, Pradeep K. Nagaraja, Archana S. Dorniak, Piotr L. Pallikuth, Sandeep Waters, Christopher M. Sood, Anil Rao, RadhaKrishna Univ Tennessee Ctr Hlth Sci Dept Physiol Memphis TN 38163 USA M D Anderson Canc Ctr Dept Gynecol Oncol Houston TX USA M D Anderson Canc Ctr Ctr RNA Interference & Non Coding RNA Houston TX USA

The role of reactive oxygen species (ROS) in osmotic stress, dextran sulfate sodium (DSS) and cyclic stretch-induced tight junction (TJ) disruption was investigated in Caco-2 cell monolayers in vitro and restraint stress-induced barrier dysfunction in mouse colon in vivo. Live cell imaging showed that osmotic stress, cyclic stretch and DSS triggered rapid production of ROS in Caco-2 cell monolayers, which was blocked by depletion of intracellular Ca2+ by 1,2-bis-(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. Knockdown of Ca(V)1.3 or TRPV6 channels blocked osmotic stress and DSS-induced ROS production and attenuated TJ disruption and barrier dysfunction. N-Acetyl L-cysteine (NAC) and L-N-G-Nitroarginine methyl ester ( L-NAME) blocked stress-induced TJ disruption and barrier dysfunction. NAC and L-NAME also blocked stress-induced activation of c-Jun N- terminal kinase (JNK) and c-Src. ROS was colocalized with the mitochondrial marker in stressed cells. Cyclosporin A blocked osmotic stress and DSS-induced ROS production, barrier dysfunction, TJ disruption and JNK activation. Mitochondria-targeted Mito-TEMPO blocked osmotic stress and DSS-induced barrier dysfunction and TJ disruption. Chronic restraint stress in mice resulted in the elevation of intracellular Ca2+, activation of JNK and c-Src, and disruption of TJ in the colonic epithelium. Furthermore, corticosterone administration induced JNK and c-Src activation, TJ disruption and protein thiol oxidation in colonic mucosa. The present study demonstrates that oxidative stress is a common signal in the mechanism of TJ disruption in the intestinal epithelium by different types of cellular stress in vitro and bio behavioral stress in vivo.

关键词： adherens junction barrier function epithelium intestine ROS tight junction

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Correction: Ribosomal modification protein rimK-like family member A activates betaine-homocysteine S-methyltransferase 1 to ameliorate hepatic steatosis

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Signal Transduction and Targeted Therapy 2025年第1期10卷 471-472页

作者： Han Yan Wenjun Liu Rui Xiang Xin Li Song Hou Luzheng Xu Lin Wang Dong Zhao Xingkai Liu Guoqing Wang Yujing Chi Jichun Yang Department of Physiology and Pathophysiology School of Basic Medical Sciences State Key Laboratory of Vascular Homeostasis and Remodeling Center for Non-coding RNA Medicine Peking University Health Science Center Beijing China Department of Endocrinology The Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou China Department of Cardiology Peking University Third Hospital Beijing China Medical and Health Analysis Center Peking University Beijing China Department of Hepatobiliary Surgery Xi-Jing Hospital Fourth Military Medical University Xi’an China Department of Endocrinology Beijing Luhe Hospital Capital Medical University Beijing China Department of Hepatobiliary and Pancreatic Surgery General Surgery Centre First Hospital of Jilin University Changchun China Key Laboratory of Pathobiology Ministry of Education College of Basic Medical Sciences Jilin University Changchun China Department of Central Laboratory and Institute of Clinical Molecular Biology Department of Gastroenterology Peking University People’s Hospital Beijing China

Correction to:Signal Transduction and Targeted Therapy https://***/10.1038/s41392-024-01914-0,published online 08 August 2024 In the process of collating the raw data,the authors noticed one inadvertent mistake in supplementaryfigure 9f after online publication of the ***β-actin in supplementaryfigure 9d was repeatedly inserted asβ-actin(upper)in supplementaryfigure *** correct data and corresponding original image are provided as *** correction does not affect the keyfindings(the existing published results or the discussion).The original article has been corrected.

关键词： hepatic correction repeatedly

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Key questions about the checkpoint blockade-are micrornas an answer?

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Cancer Biology & Medicine 2018年第2期15卷 103-115页

作者： Mihnea Dragomir Baoqing Chen Xiao Fu George A.Calin Department of Experimental Therapeutics The University of Texas MD Anderson Cancer Center Research Center for Functional Genomics Biomedicine and Translational MedicineIuliu Hatieganu University of Medicine and Pharmacy Department of Surgery Fundeni Clinical HospitalCarol Davila University of Medicine and Pharmacy Center for RNA Interference and Non-coding RNAs The University of Texas MD Anderson Cancer Center

The introduction of immune-checkpoint blockade in the cancer therapy led to a paradigm change of the management of late stage cancers. There are already multiple FDA approved checkpoint inhibitors and many other agents are undergoing phase 2 and early phase 3 clinical trials. The therapeutic indication of immune checkpoint inhibitors expanded in the last years, but still remains unclear who can benefit. Micro rnas are small rnas with no coding potential. By complementary pairing to the 3' untranslated region of messenger rna, micrornas exert posttranscriptional control of protein expression. A network of micrornas directly and indirectly controls the expression of checkpoint receptors and several micrornas can target multiple checkpoint molecules,mimicking the therapeutic effect of a combined immune checkpoint blockade. In this review, we will describe the micrornas that control the expression of immune checkpoints and we will present four specific issues of the immune checkpoint therapy in cancer:(1) imprecise therapeutic indication,(2) difficult response evaluation,(3) numerous immunologic adverse-events, and(4)the absence of response to immune therapy. Finally, we propose micrornas as possible solutions for these pitfalls. We consider that in the near future micrornas could become important therapeutic partners of the immune checkpoint therapy.

关键词： Microrna PD-1 PD-L1 CTLA-4 checkpoint inhibitors

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