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学者姓名：杨宇丰
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荧光蛋白能够将分子分布与超微结构联系起来,对于光电关联(CLEM)技术的应用至关重要.然而,常规的绿色荧光蛋白及其变体在活体组织的电子显微镜(EM)制样过程中,常因诸多不可控因素导致荧光信号显著减弱,这限制了它们作为光电关联分子探针的应用.本研究在果蝇大脑神经束膜胶质细胞中特异性表达多种GFP变体(mEmerald、hfYFP、mhYFP和CoGFPv0),以评估它们在活体组织光电关联中的应用潜力.通过提高表达量和靶向线粒体等策略,本研究最终筛选出适用于CLEM技术在果蝇神经系统研究中的CoGFPv0.本工作表明,CoGFPv0可作为一种具有良好应用前景的光电关联分子探针,特别适用于复杂的活体组织环境.
Keyword ：
CoGFPv0 CoGFPv0 GFP变体 GFP变体 光电关联技术 光电关联技术 果蝇 果蝇 荧光蛋白 荧光蛋白
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| GB/T 7714 | 陈捷 , 石丹妮 , 齐佳苗 et al. 利用果蝇模型筛选可用于动物组织光电关联的绿色荧光蛋白变体 [J]. | 电子显微学报 , 2025 , 44 (1) : 81-90 . |
| MLA | 陈捷 et al. "利用果蝇模型筛选可用于动物组织光电关联的绿色荧光蛋白变体" . | 电子显微学报 44 . 1 (2025) : 81-90 . |
| APA | 陈捷 , 石丹妮 , 齐佳苗 , 孙玲 , 杨宇丰 , 王道彪 . 利用果蝇模型筛选可用于动物组织光电关联的绿色荧光蛋白变体 . | 电子显微学报 , 2025 , 44 (1) , 81-90 . |
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Rabs are involved in neuronal development and protrusion formation. Existing studies support the notion that manipulation or mutation of Rab genes could lead to functional changes in neurons. However, whether Rabs gene-manipulation induced Drosophila eye-degeneration remains unknown. By down-regulating Rab5, but not Rab7, we first constructed a compound eye injury model in Drosophila. As the distribution, content, and even maturation of Rab5-positive endosomes are influenced by cytoskeletal proteins, like actin or tubulin-related proteins, the existence of a bidirectional regulatory relationship between Rab5 and the cytoskeleton remains unclear and worth researching. Through complete transcriptome sequencing combined immunofluorescence testing, we confirmed that down-regulation of Rab5 affected the increase of alpha-Tub84B (alternatively named TubA84B) but not gamma-tubulin. Based on Weighted Gene Co-Expression Network Analysis (WGCNA) and multitissue screening verification, this study proposes that the apoptosis-related factors-Rab5-TubA84B have conserved regulatory functions with cooperative expression. Gene manipulation confirmed that apoptotic factors, especially rpr, strongly regulate Rab5, and may ultimately influence microtubule structure through complex routes, including the Rab5 variance and the intracellular configuration ratio of alpha-Tubulin to Glyceraldehyde-3phosphate dehydrogenase.
Keyword ：
Cytoskeleton, microtubule, alpha-Tub84B, rpr Cytoskeleton, microtubule, alpha-Tub84B, rpr Drosophila Drosophila Endosome Endosome Rab5 Rab5
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| GB/T 7714 | Nan, Yuyu , Lin, Jingjing , Wei, Zaiwa et al. Microtubule-Rab5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model [J]. | CELLULAR SIGNALLING , 2025 , 127 . |
| MLA | Nan, Yuyu et al. "Microtubule-Rab5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model" . | CELLULAR SIGNALLING 127 (2025) . |
| APA | Nan, Yuyu , Lin, Jingjing , Wei, Zaiwa , Yang, Yufeng , Li, Qinghua . Microtubule-Rab5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model . | CELLULAR SIGNALLING , 2025 , 127 . |
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Aggregation of aberrant proteins is a common pathological hallmark in neurodegeneration such as polyglutamine (polyQ) and other repeat-expansion diseases. Here through overexpression of ataxin3 C-terminal polyQ expansion in Drosophila gut enterocytes, we generated an intestinal obstruction model of spinocerebellar ataxia type3 (SCA3) and reported a new role of nuclear-associated endosomes (NAEs)-the delivery of polyQ to the nucleoplasm. In this model, accompanied by the prominently increased RAB5-positive NAEs are abundant nucleoplasmic reticulum enriched with polyQ, abnormal nuclear envelope invagination, significantly reduced endoplasmic reticulum, indicating dysfunctional nucleocytoplasmic trafficking and impaired endomembrane organization. Consistently, Rab5 but not Rab7 RNAi further decreased polyQ-related NAEs, inhibited endomembrane disorganization, and alleviated disease model. Interestingly, autophagic proteins were enriched in polyQ-related NAEs and played non-canonical autophagic roles as genetic manipulation of autophagic molecules exhibited differential impacts on NAEs and SCA3 toxicity. Namely, the down-regulation of Atg1 or Atg12 mitigated while Atg5 RNAi aggravated the disease phenotypes both in Drosophila intestines and compound eyes. Our findings, therefore, provide new mechanistic insights and underscore the fundamental roles of endosome-centered nucleocytoplasmic trafficking and homeostatic endomembrane allocation in the pathogenesis of polyQ diseases.
Keyword ：
Autophagy Autophagy Endosome Endosome Inclusion body Inclusion body Non-canonical role of ATG Non-canonical role of ATG Nucleocytoplasmic trafficking Nucleocytoplasmic trafficking Spinocerebellar ataxia Spinocerebellar ataxia
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| GB/T 7714 | Nan, Yuyu , Chen, Wenfeng , Chen, Fei et al. Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity [J]. | CELL BIOLOGY AND TOXICOLOGY , 2024 , 40 (1) . |
| MLA | Nan, Yuyu et al. "Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity" . | CELL BIOLOGY AND TOXICOLOGY 40 . 1 (2024) . |
| APA | Nan, Yuyu , Chen, Wenfeng , Chen, Fei , Wei, Lili , Zeng, Aiyuan , Lin, Xiaohui et al. Endosome mediated nucleocytoplasmic trafficking and endomembrane allocation is crucial to polyglutamine toxicity . | CELL BIOLOGY AND TOXICOLOGY , 2024 , 40 (1) . |
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Royal jelly (RJ) is a biologically active substance secreted by the hypopharyngeal and mandibular glands of worker honeybees. It is widely claimed that RJ reduces oxidative stress. However, the antioxidant activity of RJ has mostly been determined by in vitro chemical detection methods or by external administration drugs that cause oxidative stress. Whether RJ can clear the endogenous production of reactive oxygen species (ROS) in cells remains largely unknown. Here, we systematically investigated the antioxidant properties of RJ using several endogenous oxidative stress models of Drosophila. We found that RJ enhanced sleep quality of aging Drosophila, which is decreased due to an increase of oxidative damage with age. RJ supplementation improved survival and suppressed ROS levels in gut cells of flies upon exposure to hydrogen peroxide or to the neurotoxic agent paraquat. Moreover, RJ supplementation moderated levels of ROS in endogenous gut cells and extended lifespan after exposure of flies to heat stress. Sleep deprivation leads to accumulation of ROS in the gut cells, and RJ attenuated the consequences of oxidative stress caused by sleep loss and prolonged lifespan. Mechanistically, RJ prevented cell oxidative damage caused by heat stress or sleep deprivation, with the antioxidant activity in vivo independent of Keap1/Nrf2 signaling. RJ supplementation activated oxidoreductase activity in the guts of flies, suggesting its ability to inhibit endogenous oxidative stress and maintain health, possibly in humans.
Keyword ：
antioxidant antioxidant biological oxidations biological oxidations Drosophila Drosophila oxidative stress oxidative stress royal jelly royal jelly sleep loss sleep loss
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| GB/T 7714 | Wen, Dongjing , Xie, Jiayu , Yuan, Yao et al. The endogenous antioxidant ability of royal jelly in Drosophila is independent of Keap1/Nrf2 by activating oxidoreductase activity [J]. | INSECT SCIENCE , 2023 , 31 (2) : 503-523 . |
| MLA | Wen, Dongjing et al. "The endogenous antioxidant ability of royal jelly in Drosophila is independent of Keap1/Nrf2 by activating oxidoreductase activity" . | INSECT SCIENCE 31 . 2 (2023) : 503-523 . |
| APA | Wen, Dongjing , Xie, Jiayu , Yuan, Yao , Shen, Lirong , Yang, Yufeng , Chen, Wenfeng . The endogenous antioxidant ability of royal jelly in Drosophila is independent of Keap1/Nrf2 by activating oxidoreductase activity . | INSECT SCIENCE , 2023 , 31 (2) , 503-523 . |
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Biological pattern formation ensures that tissues and organs develop in the correct place and orientation within the body. A great deal has been learned about cell and tissue staining techniques, and today's microscopes can capture digital images. A light microscope is an essential tool in biology and medicine. Analyzing the generated images will involve the creation of unique analytical techniques. Digital images of the material before and after deformation can be compared to assess how much strain and displacement the material responds. Furthermore, this article proposes Development Biology Patterns using Digital Image Technology (DBP-DIT) to cell image data in 2D, 3D, and time sequences. Engineered materials with high stiffness may now be characterized via digital image correlation. The proposed method of analyzing the mechanical characteristics of skin under various situations, such as one direction of stress and temperatures in the hundreds of degrees Celsius, is achievable using digital image correlation. A DBP-DIT approach to biological tissue modeling is based on digital image correlation (DIC) measurements to forecast the displacement field under unknown loading scenarios without presupposing a particular constitutive model form or owning knowledge of the material microstructure. A data-driven approach to modeling biological materials can be more successful than classical constitutive modeling if adequate data coverage and advice from partial physics constraints are available. The proposed procedures include a wide range of biological objectives, experimental designs, and laboratory preferences. The experimental results show that the proposed DBP-DIT achieves a high accuracy ratio of 99,3%, a sensitivity ratio of 98.7%, a specificity ratio of 98.6%, a probability index of 97.8%, a balanced classification ratio of 97.5%, and a low error rate of 38.6%.
Keyword ：
biology patterns biology patterns data-driven data-driven digital image correlation digital image correlation medicine medicine microscopes microscopes
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| GB/T 7714 | Ni, Shiwei , Chen, Fei , Chen, Guolong et al. Mathematical model and genomics construction of developmental biology patterns using digital image technology [J]. | FRONTIERS IN GENETICS , 2022 , 13 . |
| MLA | Ni, Shiwei et al. "Mathematical model and genomics construction of developmental biology patterns using digital image technology" . | FRONTIERS IN GENETICS 13 (2022) . |
| APA | Ni, Shiwei , Chen, Fei , Chen, Guolong , Yang, Yufeng . Mathematical model and genomics construction of developmental biology patterns using digital image technology . | FRONTIERS IN GENETICS , 2022 , 13 . |
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Polyglutamine (polyQ)-mediated mitochondria damage is one of the prime causes of polyQ toxicity, which leads to the loss of neurons and the injury of non-neuronal cells. With the discovery of the crucial role of the gut-brain axis and gut microbes in neurological diseases, the relationship between visceral damage and neurological disorders has also received extensive attention. This study successfully simulated the polyQ mitochondrial damage model by expressing 78 or 84 polyglutamine-containing Ataxin3 proteins in Drosophila intestinal enterocytes. In vivo, polyQ expression can reduce mitochondrial membrane potential, mitochondrial DNA damage, abnormal mitochondrial morphology, and loose mitochondrial cristae. Expression profiles evaluated by RNA-seq showed that mitochondrial structural genes and functional genes (oxidative phosphorylation and tricarboxylic acid cycle-related) were significantly down-regulated. More importantly, Bioinformatic analyses demonstrated that pathological polyQ expression induced vitamin B6 metabolic pathways abnormality. Active vitamin B6 participates in hundreds of enzymatic reactions and is very important for maintaining mitochondria?s activities. In the SCA3 Drosophila model, Vitamin B6 supplementation significantly suppressed ECs mitochondria damage in guts and inhibited cellular polyQ aggregates in fat bodies, indicating a promising therapeutic strategy for the treatment of polyQ. Taken together, our results reveal a crucial role for the Vitamin B6-mediated mitochondrial protection in polyQ-induced cellular toxicity, which provides strong evidence for this process as a drug target in polyQ diseases treatment.
Keyword ：
Lifespan Lifespan Mitochondria Mitochondria Polyglutamine Polyglutamine Spinocerebellar ataxia 3 Spinocerebellar ataxia 3 Vitamin B6 Vitamin B6
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| GB/T 7714 | Nan, Yuyu , Lin, Jingjing , Cui, Ying et al. Protective role of vitamin B6 against mitochondria damage in Drosophila models of SCA3 [J]. | NEUROCHEMISTRY INTERNATIONAL , 2021 , 144 . |
| MLA | Nan, Yuyu et al. "Protective role of vitamin B6 against mitochondria damage in Drosophila models of SCA3" . | NEUROCHEMISTRY INTERNATIONAL 144 (2021) . |
| APA | Nan, Yuyu , Lin, Jingjing , Cui, Ying , Yao, Jinpeng , Yang, Yufeng , Li, Qinghua . Protective role of vitamin B6 against mitochondria damage in Drosophila models of SCA3 . | NEUROCHEMISTRY INTERNATIONAL , 2021 , 144 . |
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Background: Alzheimer's disease (AD) is a common cause of dementia among elderly people. Hyperphosphorylation and aggregation of tau correlates with the clinical progression of AD; therefore, therapies targeting the aggregation of tau may have potential applications for anti-AD drug development. Several inhibitors of tau aggregation, including small molecules and antibodies, have been found to decrease the aggregation of tau and the corresponding pathology. Objective: To screen one kind of single-chain variable fragment (scFv) antibody which could inhibit the aggregation of tau and ameliorate its cytotoxicity. Methods/Results: Using phosphorylated tau (pTau) as an antigen, we obtained a scFv antibody via the screening of a high-capacity phage antibody library. Biochemical analysis revealed that this scFv antibody (scFv T1) had a strong ability to inhibit pTau aggregation both in dilute solutions and under conditions of macromolecular crowding. ScFv T1 could also depolymerize preformed pTau aggregates in vitro. Furthermore, scFv T1 was found to be able to inhibit the cytotoxicity of extracellular pTau aggregates and ameliorate tau-mediated toxicity when coexpressed with a hTauR406W mutant in the eye of transgenic Drosophila flies. Conclusion: This scFv T1 antibody may be a potential new therapeutic agent against AD. Our methods can be used to develop novel strategies against protein aggregation for the treatment of neurodegenerative diseases.
Keyword ：
Aggregation Aggregation Alzheimer's disease Alzheimer's disease Drosophila Drosophila single-chain variable fragment antibody single-chain variable fragment antibody tau tau tauopathy tauopathy toxicity toxicity
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| GB/T 7714 | Li, Sen , Yi, Yushan , Cui, Ke et al. A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo [J]. | JOURNAL OF ALZHEIMERS DISEASE , 2021 , 79 (4) : 1613-1629 . |
| MLA | Li, Sen et al. "A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo" . | JOURNAL OF ALZHEIMERS DISEASE 79 . 4 (2021) : 1613-1629 . |
| APA | Li, Sen , Yi, Yushan , Cui, Ke , Zhang, Yanqiu , Chen, Yange , Han, Dou et al. A Single-Chain Variable Fragment Antibody Inhibits Aggregation of Phosphorylated Tau and Ameliorates Tau Toxicity in vitro and in vivo . | JOURNAL OF ALZHEIMERS DISEASE , 2021 , 79 (4) , 1613-1629 . |
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Reactive oxygen species (ROS) contribute to cellular redox environment and serve as signaling molecules. Excessive ROS can lead to oxidative stress that are involved in a broad spectrum of physiological and pathological conditions. Stem cells have unique ROS regulation while cancer cells frequently show a constitutive oxidative stress that is associated with the invasive phenotype. Antioxidants have been proposed to forestall tumor progression while targeted oxidants have been used to destroy tumor cells. However, the delicate beneficial range of ROS levels for stem cells and tumor cells under distinct contexts remains elusive. Here, we used Drosophila midgut intestinal stem cell (ISCs) as an in vivo model system to tackle this question. The ROS levels of ISCs remained low in comparison to that of differentiated cells and increased with ageing, which was accompanied by elevated proliferation of ISCs in aged Drosophila. Neither upregulation nor downregulation of ROS levels significantly affected ISCs, implicating an intrinsic homeostatic range of ROS in ISCs. Interestingly, we observed similar moderately elevated ROS levels in both tumor-like ISCs induced by Notch (N) depletion and extracellular matrix (ECM)-deprived ISCs induced by p-integrin (mys) depletion. Elevated ROS levels further promoted the proliferation of tumor-like ISCs while reduced ROS levels suppressed the hyperproliferation phenotype; on the other hand, further increased ROS facilitated the survival of ECM-deprived ISCs while reduced ROS exacerbated the loss of ECM-deprived ISCs. However, N- and mys-depleted ISCs, which resembled metastatic tumor cells, harbored even higher ROS levels and were subjected to more severe cell loss, which could be partially prevented by ectopic supply of antioxidant enzymes, implicating a delicate pro-surviving and proliferating range of ROS levels for ISCs. Taken together, our results revealed stem cells can differentially respond to distinct ROS levels under various conditions and suggested that the antioxidant-based intervention of stem cells and tumors should be formulated with caution according to the specific situations.
Keyword ：
Drosophila Drosophila Integrin Integrin Intestinal stem cell Intestinal stem cell Notch Notch Reactive oxygen species Reactive oxygen species Tumor Tumor
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| GB/T 7714 | Chen, Fei , Su, Run , Ni, Shiwei et al. Context-dependent responses of Drosophila intestinal stem cells to intracellular reactive oxygen species [J]. | REDOX BIOLOGY , 2021 , 39 . |
| MLA | Chen, Fei et al. "Context-dependent responses of Drosophila intestinal stem cells to intracellular reactive oxygen species" . | REDOX BIOLOGY 39 (2021) . |
| APA | Chen, Fei , Su, Run , Ni, Shiwei , Liu, Yan , Huang, Jiexiang , Li, Gege et al. Context-dependent responses of Drosophila intestinal stem cells to intracellular reactive oxygen species . | REDOX BIOLOGY , 2021 , 39 . |
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Site-specific DNA double-strand breaks have been used to generate knock-in through the homology-dependent or -independent pathway. However, low efficiency and accompanying negative impacts such as undesirable indels or tumorigenic potential remain problematic. In this study, we present an enhanced reduced-risk genome editing strategy we named as NEO, which used either site-specific trans or cis double-nicking facilitated by four bacterial recombination factors (RecOFAR). In comparison to currently available approaches, NEO achieved higher knock-in (KI) germline transmission frequency (improving from zero to up to 10% efficiency with an average of 5-fold improvement for 8 loci) and 'cleaner' knock-in of long DNA fragments (up to 5.5 kb) into a variety of genome regions in zebrafish, mice and rats. Furthermore, NEO yielded up to 50% knock-in in monkey embryos and 20% relative integration efficiency in non-dividing primary human peripheral blood lymphocytes (hPBLCs). Remarkably, both on-target and off-target indels were effectively suppressed by NEO. NEO may also be used to introduce low-risk unrestricted point mutations effectively and precisely. Therefore, by balancing efficiency with safety and quality, the NEO method reported here shows substantial potential and improves the in vivo gene-editing strategies that have recently been developed.
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| GB/T 7714 | He, Xiaozhen , Chen, Wenfeng , Liu, Zhen et al. Efficient and risk-reduced genome editing using double nicks enhanced by bacterial recombination factors in multiple species [J]. | NUCLEIC ACIDS RESEARCH , 2020 , 48 (10) . |
| MLA | He, Xiaozhen et al. "Efficient and risk-reduced genome editing using double nicks enhanced by bacterial recombination factors in multiple species" . | NUCLEIC ACIDS RESEARCH 48 . 10 (2020) . |
| APA | He, Xiaozhen , Chen, Wenfeng , Liu, Zhen , Yu, Guirong , Chen, Youbang , Cai, Yi-Jun et al. Efficient and risk-reduced genome editing using double nicks enhanced by bacterial recombination factors in multiple species . | NUCLEIC ACIDS RESEARCH , 2020 , 48 (10) . |
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Aberrant mitophagy has been implicated in a broad spectrum of disorders. PINK1, Parkin, and ubiquitin have pivotal roles in priming mitophagy. However, the entire regulatory landscape and the precise control mechanisms of mitophagy remain to be elucidated. Here, we uncover fundamental mitophagy regulation involving PINK1 and a non-canonical role of the mitochondrial Tu translation elongation factor (TUFm). The mitochondrion-cytosol dual-localized TUFm interacts with PINK1 biochemically and genetically, which is an evolutionarily conserved Parkin-independent route toward mitophagy. A PINK1-dependent TUFm phosphoswitch at Ser222 determines conversion from activating to suppressing mitophagy. PINK1 modulates differential translocation of TUFm because p-S222-TUFm is restricted predominantly to the cytosol, where it inhibits-mitophagy by impeding Atg5-Atg12 formation. The self-antagonizing feature of PINK1/TUFm is critical for the robustness of mitophagy regulation, achieved by the unique kinetic parameters of p-S222-TUFm, p-S65-ubiquitin, and their common kinase PINK1. Our findings provide new mechanistic insights into mitophagy and mitophagy-associated disorders.
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| GB/T 7714 | Lin, Jingjing , Chen, Kai , Chen, Wenfeng et al. Paradoxical Mitophagy Regulation by PINK1 and TUFm [J]. | MOLECULAR CELL , 2020 , 80 (4) : 607-, . |
| MLA | Lin, Jingjing et al. "Paradoxical Mitophagy Regulation by PINK1 and TUFm" . | MOLECULAR CELL 80 . 4 (2020) : 607-, . |
| APA | Lin, Jingjing , Chen, Kai , Chen, Wenfeng , Yao, Yizhou , Ni, Shiwei , Ye, Meina et al. Paradoxical Mitophagy Regulation by PINK1 and TUFm . | MOLECULAR CELL , 2020 , 80 (4) , 607-, . |
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