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| 1 | Kinetics and mechanisms of mitotic inheritance of DNA methylation and their roles in aging-associated methylome deterioration显示文摘Mitotic inheritance of the DNA methylome is a challenging task for the maintenance of cell identity.Whether DNA methylation pattern in different genomic contexts can all be faithfully maintained is an open question.A replication-coupled DNA methylation maintenance model was proposed decades ago,but some observations suggest that a replication-uncoupled maintenance mechanism exists.However,the capacity and the underlying molecular events of replication-uncoupled maintenance are unclear.By measuring maintenance kinetics at the single-molecule level and assessing mutant cells with perturbation of various mechanisms,we found that the kinetics of replication-coupled maintenance are governed by the UHRF1–Ligase 1 and PCNA–DNMT1 interactions,whereas nucleosome occupancy and the interaction between UHRF1 and methylated H3K9 specifically regulate replication-uncoupled maintenance.Surprisingly,replication-uncoupled maintenance is sufficiently robust to largely restore the methylome when replication-coupled maintenance is severely impaired.However,solo-WCGW sites and other CpG sites displaying aging-and cancer-associated hypomethylation exhibit low maintenance efficiency,suggesting that although quite robust,mitotic inheritance of methylation is imperfect and that this imperfection may contribute to selective hypomethylation during aging and tumorigenesis. | Xuan Ming Zhuqiang Zhang Zhuoning Zou Cong Lv Qiang Dong Qixiang He Yangyang Yi Yingfeng Li Hailin Wang Bing Zhu | 2020 | Cell Research2020，30，11： | 4 |
| 2 | Author Correction: Kinetics and mechanisms of mitotic inheritance of DNA methylation and their roles in aging-associated methylome deterioration显示文摘We apologize for the mistake of the fund information in the acknowledgements.The correct information is as follows.This correction does not affect the conclusion of the work. | Xuan Ming Zhuqiang Zhang Zhuoning Zou Cong Lv Qiang Dong Qixiang He Yangyang Yi Yingfeng Li Hailin Wang Bing Zhu | 2021 | Cell Research2021，31，3： | 2 |
| 3 | Force Spectrum of Single CsgA Nanofiber Reveal Surprising Properties显示文摘CsgA protein monomers consist of aβ-helix of five repeat units possessing several conservative residues and thus,inherently fibrillate.CsgA protein monomers could self-assemble into hierarchical nanofiber structure cross multiple scales after expression and secretion by E.Coli cells.Previous researches show that CsgA nanofibers could provide adhesion,stiffness,and mechanical homogeneity for the biofilms,host cells’fibronectin binding for internalization,or protection against phage attack.CsgA nanofibers have obtained various applications in material science and synthetic biology.To illustrate,CsgA nanofibers have characteristics of intrinsic hierarchical structures across multiple scales,robustness in harsh environments and programmable functionality via biological tools.Studying the force spectrum or mechanical properties of the nanofiber can provide fundamental information of self-assembly process and ultra-stability in extreme conditions.Single molecule techniques such as atomic force microscopy,optical tweezers,and magnetic tweezers have been widely applied to study proteins.In these studies,proteins are usually chemically conjugated or genetically constructed to have a tag such as histidine,cysteine or biotin.Genetic engineering requires modification of the plasmids encoding the specific protein,and also involve special protein expression and purification.Such study needs collaboration from multi-disciplinary.It normally studies one protein at a time which gives out clear signal but lacks throughput and efficiency.Here we have established a simple method to measure all kinds of proteins without labels.The carboxyl terminus of a protein is attached to the amine group on a magnetic bead,and the amine terminus of the protein is attached to glutaraldehyde on the glass slide.Then we used magnetic tweezers to manipulate and stretched the bead and protein.Extension versus rotation relation was used to identify a single protein or protein fibril.The fiber under tension is also observed by Scanning Electronic Microcopy which convinces that single CsgA-His fibril is linked to a microbead.The peak of diameter distribution is around 15 nm.The fracture of fibers was observed in real time on SEM.Force-extension curves of single fibers are obtained in real time.The force-extension curves generally agree with the worm like chain model.The persistence lengths from the fitting are from 0.9 to 49.8 nm.The elongation ratio increases gradually with force until reaches a plateau.The maximum elongation ratio of 78 nanofibers were made into an elongation ratio distribution diagram,more than half of CsgA-His nanofibers has an elongation ratio from 0 to 2,some are distributed in 2~10,and a few are distributed in 10~18.The maximum elongation ratio of CsgA-His nanofibers is 17.1,indicating that the fibril’s flexibility is much higher than DNA or silk fiber.For forces less than 20 pN,the extension was reversible.With a 42.1 pN holding force,the extension jumped in steps of from 30 to 365 nm and was irreversible.At the scale tested,the jumps corresponded to the unfolding of multiple beta sheets in the fiber.Work for CsgA-His nanofibers during stretching increase with the normalized strain fractions.The experimental data agree with a theoretical prediction for a single CsgA protein from a SMD calculation.Therefore,our results provide key information for the understandings of CsgA protein nanofiber assembly and biofilm robustness. | Jingqi Lv Yingfeng Li Kai Zhou Pei Guo Ke Ding Quan Long Yang Liu Qi Wang Chao Zhong Botao Xiao | 2019 | 医用生物力学2019，34，A01： | 0 |
| 4 | RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis显示文摘Hantaan virus(HTNV)is a rodent-borne virus that causes hemorrhagic fever with renal syndrome(HFRS),resulting in a high mortality rate of 15%.Interferons(IFNs)play a critical role in the anti-hantaviral immune response,and IFN pretreatment efficiently restricts HTNV infection by triggering the expression of a series of IFNstimulated genes(ISGs)through the Janus kinase-signal transducer and activator of transcription 1(JAK-STAT)pathway.However,the tremendous amount of IFNs produced during late infection could not restrain HTNV replication,and the mechanism remains unclear.Here,we demonstrated that receptor-interacting protein kinase 3(RIPK3),a crucial molecule that mediates necroptosis,was activated by HTNV and contributed to hantavirus evasion of IFN responses by inhibiting STAT1 phosphorylation.RNA-seq analysis revealed the upregulation of multiple cell death-related genes after HTNV infection,with RIPK3 identified as a key modulator of viral replication.RIPK3 ablation significantly enhanced ISGs expression and restrained HTNV replication,without affecting the expression of pattern recognition receptors(PRRs)or the production of type I IFNs.Conversely,exogenously expressed RIPK3 compromised the host's antiviral response and facilitated HTNV replication.RIPK3^(-/-)mice also maintained a robust ability to clear HTNV with enhanced innate immune responses.Mechanistically,we found that RIPK3 could bind STAT1 and inhibit STAT1 phosphorylation dependent on the protein kinase domain(PKD)of RIPK3 but not its kinase activity.Overall,these observations demonstrated a noncanonical function of RIPK3 during viral infection and have elucidated a novel host innate immunity evasion strategy utilized by HTNV. | Yue Si Haijun Zhang Ziqing Zhou Xudong Zhu Yongheng Yang He Liu Liang Zhang Linfeng Cheng Kerong Wang Wei Ye Xin Lv Xijing Zhang Wugang Hou Gang Zhao Yingfeng Lei Fanglin Zhang Hongwei Ma | 2023 | Virologica Sinica2023，38，5： | 0 |
| 5 | Studies on Stability and Moisture Retention of Urea and Its Derivatives显示文摘The effect of triethyl citrate(TEC)on the stability of cream preparations containing urea or hydroxyethyl urea along with their moisturizing effect on skin was investigated.The results showed that creams incorporating urea or hydroxyethyl urea led to increase in pH value after a long-term and high-temperature storage.pH change in the latter one was relatively smaller.With the addition of TEC,the elevated pH of the formula system was suppressed.In the situation of stable formula,the higher the TEC added,the more significant inhibition effect on the pH change was observed.In the moisture retention test in vivo,compared to 27.19%moisture rate in negative control,cream preparations containing 5%urea or 5%hydroxyethyl urea had remarkable moisturizing effect,which were all higher than 52%.The latter one was relatively more prominent.There is no significant effect on moisturizing effect for product with TEC additive. | Lv Yingfeng Lv Wanqi Zhou Jingmin | 2023 | China Detergent & Cosmetics2023，8，3： | 0 |
| 6 | STING strengthens host anti-hantaviral immunity through an interferon-independent pathway显示文摘Hantaan virus(HTNV),the prototype virus of hantavirus,could escape innate immunity by restraining type I interferon(IFN)responses.It is largely unknown whether there existed other efficient anti-hantaviral tactics in host cells.Here,we demonstrate that the stimulator of interferon genes(STING)strengthens the host IFNindependent anti-hantaviral immunity.HTNV infection activates RIG-I through IRE1-XBP 1-mediated ER stress,which further facilitates the subcellular translocation and activation of STING.During this process,STING triggers cellular autophagy by interacting with Rab7A,thus restricting viral replication.To note,the anti-hantaviral effects of STING are independent of canonical IFN signaling.Additionally,neither application of the pharmacological antagonist nor the agonist targeting STING could improve the outcomes of nude mice post HTNV challenge in vivo.However,the administration of plasmids exogenously expressing the mutant C-terminal tail(ΔCTT)STING,which would not trigger the type I IFN responses,protected the nude mice from lethal HTNV infection.In summary,our research revealed a novel antiviral pathway through the RIG-I-STING-autophagy pathway,which offered novel therapeutic strategies against hantavirus infection. | Kerong Wang Jian Zhang Yongheng Yang Yue Si Ziqing Zhou Xudong Zhu Sushan Wu He Liu Hui Zhang Liang Zhang Linfeng Cheng Wei Ye Xin Lv Yingfeng Lei Xijing Zhang Shilin Cheng Lixin Shen Fanglin Zhang Hongwei Ma | 2023 | Virologica Sinica2023，38，4： | 0 |
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