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RING-box proteins regulate leaf senescence and stomatal closure via repression of ABA transporter gene ABCG40

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Journal of Integrative Plant Biology 2022年第5期64卷 979-994页

作者： Yun Qi Wei Jun Jie Yuan Chen Chen Xiao Gui Xin Li Jing Ying Yan Shao Jian Zheng Zhong Jie Ding State Key Laboratory of Plant Physiology and Biochemistry College of Life SciencesZhejiang UniversityHangzhou 310058China Guangdong Laboratory for Lingnan Modern Agriculture College of Natural Resources and EnvironmentSouth China Agricultural UniversityGuangzhou 510642China College of Agronomy and Biotechnology Zhejiang UniversityHangzhou 310058China Agricultural Experimental Station Zhejiang UniversityHangzhou 310058China

Plant hormone abscisic acid(ABA)plays an indispensable role in the control of leaf senescence,during which ABA signaling depends on its biosynthesis.Nevertheless,the role of ABA transport in leaf senescence remains unknown.Here,we identified two novel RING-box protein-encoding genes UBIQUITIN LIGASE of senescence 1 and2(ULS1 and ULS2)involved in leaf senescence.Lack of ULS1 and ULS2 accelerates leaf senescence,which is specifically promoted by ABA treatment.Furthermore,the expression of senescence-related genes is significantly affected in mature leaves of uls1/uls2 double mutant(versus wild type(WT))in an ABA-dependent manner,and the ABA content is substantially increased.ULS1 and ULS2 are mainly expressed in the guard cells and aging leaves,and the expression is induced by ABA.Further RNA-seq and quantitative proteomics of ubiquitination reveal that ABA transporter ABCG40 is highly expressed in uls1/uls2 mutant versus WT,though it is not the direct target of ULS1/2.Finally,we show that the acceleration of leaf senescence,the increase of leaf ABA content,and the promotion of stomatal closure in uls1/usl2 mutant are suppressed by abcg40 loss-of-function mutation.These results indicate that ULS1 and ULS2 function in feedback inhibition of ABCG40-dependent ABA transport during ABA-induced leaf senescence and stomatal closure.

关键词： ABA Arabidopsis E3 ligase leaf senescence stomata transport

Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1α/NF-κB feedback pathway to inhibit liver fibrosis

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Acta Pharmaceutica Sinica B 2022年第9期12卷 3618-3638页

作者： Feixia Wang Zhanghao Li Li Chen Ting Yang Baoyu Liang Zili Zhang Jiangjuan Shao Xuefen Xu Guoping Yin Shijun Wang Hai Ding Feng Zhang Shizhong Zheng Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica School of PharmacyNanjing University of Chinese MedicineNanjing 210023China Department of General Surgery Nanjing Hospital Affiliated to Nanjing University of Chinese MedicineNanjing 210003China Department of Anesthesiology Nanjing Hospital Affiliated to Nanjing University of Chinese MedicineNanjing 210003China College of Traditional Chinese Medicine Shandong University of Traditional Chinese MedicineJinan 250035China

senescence of activated hepatic stellate cells(aHSCs) is a stable growth arrest that is implicated in liver fibrosis regression.Senescent cells often accompanied by a multi-faceted senescence-associated secretory phenotype(SASP).But little is known about how alanine-serine-cysteine transporter type-2(ASCT2),a high affinity glutamine transporter,affects HSC senescence and SASP during liver fibrosis.Here,we identified ASCT2 is mainly elevated in aHSCs and positively correlated with liver fibrosis in human and mouse fibrotic livers.We first discovered ASCT2 inhibition induced HSCs to senescence in vitro and in vivo.The proinflammatory SASP were restricted by ASCT2 inhibition at senescence initiation to prevent paracrine migration.Mechanically,ASCT2 was a direct target of glutaminolysisdependent proinflammatory SASP,interfering IL-1α/NF-κB feedback loop via interacting with precursor IL-1α at Lys82.From a translational perspective,atractylenolide Ⅲ is identified as ASCT2 inhibitor through directly bound to Asn230 of ASCT2.The presence of -OH group in atractylenolide Ⅲ is suggested to be favorable for the inhibition of ASCT2.Importantly,atractylenolide Ⅲ could be utilized to treat liver fibrosis mice.Taken together,ASCT2 controlled HSC senescence while modifying the proinflammatory SASP.Targeting ASCT2 by atractylenolide Ⅲ could be a therapeutic candidate for liver fibrosis.

关键词： Hepatic stellate cells senescence SASP ASCT2 Precursor IL-1α NF-κB Atractylenolide III Liver fibrosis

Insulin-like growth factor binding proteins 7 prevents dental pulp-derived mesenchymal stem cell senescence via metabolic downregulation of p21

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Science China(Life Sciences) 2022年第11期65卷 2218-2232页

作者： Xiaoyu Li Liang Feng Chunmei Zhang Jinsong Wang Songlin Wang Lei Hu Molecular Laboratory for Gene Therapy and Tooth Regeneration Beijing Key Laboratory of Tooth Regeneration and Function ReconstructionBeijing Laboratory of Oral HealthCapital Medical University School of StomatologyBeijing 100050China Immunology Research Center for Oral and Systemic Health Beijing Friendship HospitalCapital Medical UniversityBeijing 100050China Department of Biochemistry and Molecular Biology Capital Medical University School of Basic MedicineBeijing 100069China Laboratory for Oral and General Health Integration and Translation Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China Research Unit of Tooth Development and Regeneration Chinese Academy of Medical SciencesBeijing 100700China Department of Prosthodontics Capital Medical University School of StomatologyBeijing 100050China

Cellular senescence affects the efficacy of mesenchymal stem cells(MSCs)-mediated tissue regeneration.Insulin-like growth factor binding proteins-7(IGFBP7),as a member of the IGF family,is associated with osteogenic differentiation and the senescence of MSCs,but its exact function and mechanism remain unclear.We found IGFBP7 promoted the osteogenic differentiation and prevented the senescence of dental pulp-derived MSCs(DPSCs),as observed in the gain-of-function and lossof-function analyses,the senescence-associated marker p21 showed the most pronounced expression changes.We demonstrated that IGFBP7 activated the biological activity of SIRT1 deacetylase via metabolism,resulting in a deacetylation of H3K36ac and a decrease of the binding affinity of H3K36ac to p21 promoter,thereby reducing the transcription of p21,which ultimately prevents DPSCs senescence and promotes tissue regeneration.The activation of the mitochondrial electron transport chain(ETC)by Coenzyme Q10 could rescue the promotion of DPSC senescence induced by the knockdown of IGFBP7,whereas the inhibition of ETC by rotenone attenuated the prevention of DPSC senescence induced by IGFBP7 overexpression.In conclusion,our present results reveal a novel function of IGFBP7 in preventing DPSC senescence via the metabolism-induced deacetylation of H3K36ac and reduction of p21 transcription,suggesting that IGFBP7 is a potential target for promoting tissue regeneration in an aging environment.

关键词： dental pulp-derived mesenchymal stem cells insulin-like growth factor binding protein 7 senescence metabolism SIRT1 p21

Unveiling E2F4,TEAD1 and AP-1 as regulatory transcription factors of the replicative senescence program by multi-omics analysis

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Protein & Cell 2022年第10期13卷 742-759页

作者： Yuting Wang Liping Liu Yifan Song Xiaojie Yu Hongkui Deng School of Basic Medical Sciences State Key Laboratory of Natural and Biomimetic DrugsPeking UniversityBeijing 100191China The MOE Key Laboratory of Cell Proliferation and Differentiation College of Life SciencesPeking-Tsinghua Center for Life SciencesPeking UniversityBeijing 100871China State Key Laboratory of Chemical Oncogenomics School of Chemical Biology and BiotechnologyPeking University Shenzhen Graduate SchoolShenzhen 518055China

senescence,a stable state of growth arrest,affects many physiological and pathophysiological processes,especially aging.Previous work has indicated that transcription factors(TFs)play a role in regulating senescence.However,a systematic study of regulatory TFs during replicative senescence(RS)using multiomics analysis is still lacking.Here,we generated timeresolved RNA-seq,reduced representation bisulfite sequencing(RRBS)and ATAC-seq datasets during RS of mouse skin fibroblasts,which demonstrated that an enhanced inflammatory response and reduced proliferative capacity were the main characteristics of RS in both the transcriptome and epigenome.Through integrative analysis and genetic manipulations,we found that transcription factors E2F4,TEAD1 and AP-1 are key regulators of RS.Overexpression of E2f4 improved cellular proliferative capacity,attenuated SA-β-Gal activity and changed RS-associated differentially methylated sites(DMSs).Moreover,knockdown of Tead1 attenuated SA-β-Gal activity and partially altered the RS-associated transcriptome.In addition,knockdown of Atf3,one member of AP-1 superfamily TFs,reduced Cdkn2a(p16)expression in pre-senescent fibroblasts.Taken together,the results of this study identified transcription factors regulating the senescence program through multi-omics analysis,providing potential therapeutic targets for anti-aging.

关键词： transcription factor senescence multiomics

Inhibition of Cyclin F Promotes Cellular senescence through Cyclin-dependent Kinase 1-mediated Cell Cycle Regulation

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Current Medical Science 2023年第2期43卷 246-254页

作者： Xun LI You-jian LI Meng-jie WANG Ke-peng OU Ya-qi CHEN GI Cancer Research Institute Tongji HospitalHuazhong University of Science and TechnologyWuhan430030China College of Pharmacy National&Local Joint Engineering Research Center of Targeted and Innovative TherapeuticsChongqing Key Laboratory of Kinase Modulators as Innovative MedicineChongqing University of Arts and SciencesChongqing402160China Department of Obstetrics and Gynecology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China College of Pharmaceutical Sciences and Chinese Medicine Southwest UniversityChongqing400715China

Objective Kidney renal clear cell carcinoma(KIRC)is a common renal malignancy that has a poor prognosis.As a member of the F box family,cyclin F(CCNF)plays an important regulatory role in normal tissues and tumors.However,the underlying mechanism by which CCNF promotes KIRC proliferation still remains unclear.Methods Bioinformatics methods were used to analyze The Cancer Genome Atlas(TCGA)database to obtain gene expression and clinical prognosis data.The CCK8 assay,EdU assay,and xenograft assay were used to detect cell proliferation.The cell senescence and potential mechanism were assessed by SA-β-gal staining,Western blotting,as well as ELISA.Results Our data showed that CCNF was highly expressed in KIRC patients.Meanwhile,downregulation of CCNF inhibited cell proliferation in vivo and in vitro.Further studies showed that the reduction of CCNF promoted cell senescence by decreasing cyclin-dependent kinase 1(CDK1),increasing the proinflammatory factors interleukin(IL)-6 and IL-8,and then enhancing the expression of p21 and p53.Conclusion We propose that the high expression of CCNF in KIRC may play a key role in tumorigenesis by regulating cell senescence.Therefore,CCNF shows promise as a new biomarker to predict the clinical prognosis of KIRC patients and as an effective therapeutic target.

关键词： cyclin F kidney renal clear cell carcinoma clinical outcome cyclin-dependent kinase 1 senescence

EPAS1 prevents telomeric damage-induced senescence by enhancing transcription of TRF1,TRF2,and RAD50

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Zoological Research 2023年第3期44卷 636-649页

作者： Kai-Qin Li Gao-Jing Liu Xiu-Yun Liu Qiong-Fang Chen Xiao-Yan Huang Qiu Tu Jiao Zhang Qing Chang Yun-Hua Xie Rong Hua Dong-Ming Xu Zhen Liu Bo Zhao Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences&Yunnan Province KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common DiseasesKunming Institute of ZoologyChinese Academy of SciencesKunmingYunnan 650201China State Key Laboratory of Genetic Resources and Evolution Kunming Institute of ZoologyChinese Academy of SciencesKunmingYunnan 650201China University of Chinese Academy of Sciences Beijing 100049China Primate Facility National Research Facility for Phenotypic&Genetic Analysis of Model Animalsand National Resource Center for Non-Human PrimatesKunming Institute of ZoologyChinese Academy of SciencesKunmingYunnan 650201China

Telomeres are nucleoprotein structures located at the end of each chromosome,which function in terminal protection and genomic stability.Telomeric damage is closely related to replicative senescence in vitro and physical aging in vivo.As relatively long-lived mammals based on body size,bats display unique telomeric patterns,including the upregulation of genes involved in alternative lengthening of telomeres(ALT),DNA repair,and DNA replication.At present,however,the relevant molecular mechanisms remain unclear.In this study,we performed cross-species comparison and identified EPAS1,a well-defined oxygen response gene,as a key telomeric protector in bat fibroblasts.Bat fibroblasts showed high expression of EPAS1,which enhanced the transcription of shelterin components TRF1 and TRF2,as well as DNA repair factor RAD50,conferring bat fibroblasts with resistance to senescence during long-term consecutive expansion.Based on a human single-cell transcriptome atlas,we found that EPAS1 was predominantly expressed in the human pulmonary endothelial cell subpopulation.Using in vitro-cultured human pulmonary endothelial cells,we confirmed the functional and mechanistic conservation of EPAS1 in telomeric protection between bats and humans.In addition,the EPAS1 agonist M1001 was shown to be a protective compound against bleomycin-induced pulmonary telomeric damage and senescence.In conclusion,we identified a potential mechanism for regulating telomere stability in human pulmonary diseases associated with aging,drawing insights from the longevity of bats.

关键词： Bat Telomere senescence EPAS1 M1001 Pulmonary endothelial cell

A petunia transcription factor, PhOBF1, regulates flower senescence by modulating gibberellin biosynthesis

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Horticulture Research 2023年第4期10卷 38-52页

作者： Xiaotong Ji Ziwei Xin Yanping Yuan Meiling Wang Xinyi Lu Jiaqi Li Yanlong Zhang Lixin Niu Cai-Zhong Jiang Daoyang Sun College of Landscape Architecture and Arts Northwest A&F UniversityYanglingShaanxi 712100China Department of Plant Sciences University of CaliforniaDavisDavisCA 95616USA Crops Pathology and Genetics Research Unit USDA-ARSDavisCA 95616USA

Flower senescence is commonly enhanced by the endogenous hormone ethylene and suppressed by the gibberellins(GAs)in plants.However,the detailed mechanisms for the antagonism of these hormones during f lower senescence remain elusive.In this study,we characterized one up-regulated gene PhOBF1,belonging to the basic leucine zipper transcription factor family,in senescing petals of petunia(Petunia hybrida).Exogenous treatments with ethylene and GA3 provoked a dramatic increase in PhOBF1 transcripts.Compared with wild-type plants,PhOBF1-RNAi transgenic petunia plants exhibited shortened f lower longevity,while overexpression of PhOBF1 resulted in delayed flower senescence.Transcript abundances of two senescence-related genes PhSAG12 and PhSAG29 were higher in PhOBF1-silenced plants but lower in PhOBF1-overexpressing plants.Silencing and overexpression of PhOBF1 affected expression levels of a few genes involved in the GA biosynthesis and signaling pathways,as well as accumulation levels of bioactive GAs GA1 and GA3.Application of GA3 restored the accelerated petal senescence to normal levels in PhOBF1-RNAi transgenic petunia lines,and reduced ethylene release and transcription of three ethylene biosynthetic genes PhACO1,PhACS1,and PhACS2.Moreover,PhOBF1 was observed to specifically bind to the PhGA20ox3 promoter containing a G-box motif.Transient silencing of PhGA20ox3 in petunia plants through tobacco rattle virus-based virus-induced gene silencing method led to accelerated corolla senescence.Our results suggest that PhOBF1 functions as a negative regulator of ethylene-mediated f lower senescence by modulating the GA production.

关键词： senescence pet flower

Integrative analysis of transcriptome reveals the possible mechanism of delayed leaf senescence in pak choi(Brassica rapa subsp.chinensis)following melatonin treatment

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Food Quality and Safety 2023年第1期7卷 87-99页

作者：刘雪松李韫同朱俊臻李鹏霞 Institute of Agricultural Facilities and Equipment Jiangsu Academy of Agricultural SciencesNanjingChina Key Laboratory of Cold Chain Logistics Technology for Agro-Products Ministry of Agriculture and Rural AffairsChina Department of Food Science Shenyang Agricultural UniversityShenyangChina School of Food and Biological Engineering Jiangsu UniversityZhenjiangChina Jiangsu Key Laboratory for Horticultural Crop Genetic Improvement NanjingChina

Melatonin(MT)is a low molecular weight compound with a wide variety of biological functions in plants.It is known to delay senescence in various fruits and vegetables.This study demonstrates that MT(100μmol/L)delayed the senescence of pak choi stored at 20°C.A total of 1121 differentially expressed genes(DEGs)were identified in an MT-treated group in comparison to untreated pak choi.Analysis of DEGs revealed that MT-induced delay in senescence involved reduction in the expression of chlorophyll metabolism genes and regulation of the expression of hormone-related genes and leaf senescence-related transcription factors.MT decreased the activity of chlorophyll metabolism-related enzymes Mg-dechelatase,pheophytinase,and pheide a oxygenase,decreased the concentrations of abscisic acid and jasmonic acid,and increased auxin concentration.MT delayed the impact of senescence-related transcription factors BcNAC41 and BcNAC87 on tobacco leaf senescence.This study provides an insight into the molecular mechanisms of MT-induced delay of postharvest senescence in pak choi and confirms its potential as a preservation technique.

关键词： Pak choi melatonin transcriptome postharvest senescence

Photosynthetic properties of the mid-vein and leaf lamina of field-grown, high-yield hybrid rice during senescence

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Journal of Integrative Agriculture 2022年第7期21卷 1913-1926页

作者： GAO Zhi-ping XU Min-li ZHANG Hai-zi Lü Chuan-gen CHEN Guo-xiang College of Life Sciences Nanjing Normal UniversityNanjing 210023P.R.China Institute of Food and Crops Jiangsu Academy of Agricultural SciencesNanjing 210014P.R.China

Previous studies with rice(Oryza sativa L.) have shown that the different components of the photosynthetic apparatus are not uniformly synthesized or degraded during senescence. However, while most of those studies have focused on the leaf lamina, few have addressed senescence-associated chloroplast function or leaf physiology. Here, we investigated the photosynthetic properties of the mid-vein and leaf lamina in a high-yield hybrid rice cultivar(Liangyoupei 9, LYP9) during the senescence stage. Assimilation and transpiration decreased more slowly in the mid-vein than in the lamina during senescence, suggesting more sustained photosynthesis in the mid-vein, as well as stronger heat dissipation. Two-dimensional gel electrophoresis suggested that photosynthesis and energy metabolism were less affected by senescence in the mid-vein than in the leaf lamina. During late senescence, the excess energy dissipation in the midvein through the xanthophyll cycle had a higher active photosynthetic capacity than in the leaf lamina, and we inferred that the mid-vein and leaf lamina of LYP9 rice differed in terms of their maturation. Taken together, these results provide new insights into the underlying mechanisms of senescence of the rice mid-vein and associated physiology.

关键词： mid-vein rice photosynthetic properties senescence