期刊：
JOURNAL OF PROTEOME RESEARCH,2022年21(8):1939-1947 ISSN：1535-3893
通讯作者：
Cuihong Wan
作者机构：
[Wan, Cuihong; Pan, Ni; Sun, Yan; Huang, Jiangmei; Wang, Zhiwei] Cent China Normal Univ, Sch Life Sci, Wuhan 430079, Hubei, Peoples R China.;[Wan, Cuihong; Pan, Ni; Sun, Yan; Huang, Jiangmei; Wang, Zhiwei] Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Cuihong Wan] S;School of Life Sciences and Hubei Key Laboratory of Genetic Regulation and Integrative Biology, Central China Normal University, Wuhan, Hubei 430079, People’s Republic of China
摘要：
Small open reading frame-encoded peptides (SEPs) are microproteins with a length of 100 amino acids or less, which may play a critical role in maintaining cell homeostasis under stress. Therefore, we used mass spectrometry-based proteomics to explore microproteins potentially involved in cellular stress responses in Saccharomyces cerevisiae. A total of 225 microproteins with 1920 unique peptides were identified under six culture conditions: normal, oxidation, starvation, ultraviolet radiation, heat shock, and heat shock with starvation. Among these microproteins, we found 70 SEPs with 75 unique peptides. The annotated microproteins are involved in stress-related processes, such as cell redox reactions, cell wall modification, protein folding and degradation, and DNA damage repair. It suggests that SEPs may also play similar functions under stress conditions. For example, SEP IP_008057, translated from a short coding sequence of YJL159W, may play a role in heat shock. This study identified stress-responsive SEPs in S. cerevisiae and provided valuable information to determine the functions of these proteins, which enrich the genome and proteome of S. cerevisiae and show clues to improving the stress tolerance of S. cerevisiae.
作者机构：
[Wan, Cuihong; Wan, CH] Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.;Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Hubei, Peoples R China.
通讯机构：
[Wan, CH ] C;Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.
期刊：
Journal of Fungi,2022年8(7):667- ISSN：2309-608X
通讯作者：
Yongze Yuan
作者机构：
[Li, Guoqi; Liu, Deli; Wu, Lijuan; Cuan, Rongrong; Yuan, Yongze; Wang, Xiao] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Peoples R China.;[Liu, Shaoting] Cent China Normal Univ, Sch Publ Adm, Wuhan 430079, Peoples R China.;[Zheng, Yongliang] Huanggang Normal Univ, Coll Biol & Agr Resources, Hubei Collaborat Innovat Ctr Characterist Resourc, Hubei Key Lab Econ Forest Germplasm Improvement &, Huanggang 438000, Peoples R China.
通讯机构：
[Yongze Yuan] H;Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, China<&wdkj&>Author to whom correspondence should be addressed.
关键词：
P. italicum;calcium/calmodulin-dependent protein kinase (CaMK);conidiation;virulence;stress tolerance;transcriptome
期刊：
Journal of Inflammation,2022年19(1):1-13 ISSN：1476-9255
通讯作者：
He, Xianghu;Wu, Gang;Wang, Zhihua
作者机构：
[Guo, Ningning; Fang, Yu; Wu, Gang; Mao, Shuai; Lv, Jian] Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan 430061, Peoples R China.;[Guo, Ningning; Fang, Yu; Wang, Zhihua; Lv, Jian] Chinese Acad Med Sci, Shenzhen Key Lab Cardiovasc Dis, Fuwai Hosp, Shenzhen 518057, Peoples R China.;[Guo, Ningning; Fang, Yu; Wang, Zhihua; Lv, Jian] Chinese Acad Med Sci & Peking Union Med Coll, Fuwai Hosp, Natl Ctr Cardiovasc Dis, State Key Lab Cardiovasc Dis, Beijing 100037, Peoples R China.;[Chen, Meng; He, Xianghu] Wuhan Univ, Dept Anesthesiol, Zhongnan Hosp, Wuhan 430071, Peoples R China.;[Tong, Jingjing] Cent China Normal Univ, Sch Life Sci, Wuhan 430068, Peoples R China.
通讯机构：
[He, Xianghu; Wu, Gang] D;[Wang, Zhihua] S;Department of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.;Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430061, China.;Shenzhen Key Laboratory of Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, Shenzhen, 518057, China.
摘要：
Severe sepsis and its subsequent complications cause high morbidity and mortality rates worldwide. The lung is one of the most vulnerable organs sensitive to the sepsis-associated inflammatory storm and usually develops into acute respiratory distress syndrome (ARDS)/acute lung injury (ALI). The pathogenesis of sepsis-associated ALI is accompanied by coordinated transmembrane signal transduction and subsequent programmed cell death; however, the underlying mechanism remains largely unclear. Here we find that the expression of serine incorporator 2 (Serinc2), a protein involved in phosphatidylserine synthesis and membrane incorporation, is upregulated in cecal ligation and puncture (CLP)-induced ALI. Furthermore, the Serinc2-knockout (KO) mouse line is generated by the CRISPR-cas9 approach. Compared with wild-type mice, the Serinc2-KO mice exhibit exacerbated ALI-related pathologies after CLP. The expressions of pro-inflammatory factors, including IL1β, IL6, TNFα, and MCP1, are significantly enhanced by Serinc2 deficiency, concurrent with over-activation of STAT3, p38 and ERK pathways. Conversely, Serinc2 overexpression in RAW264.7 cells significantly suppresses the inflammatory responses induced by lipopolysaccharide (LPS). Serinc2 KO aggravates CLP-induced apoptosis as evidenced by increases in TUNEL-positive staining, Bax expression, and cleaved caspase-3 and decreases in BCL-2 expression and Akt phosphorylation, whereas these changes are suppressed by Serinc2 overexpression in LPS-treated RAW264.7 cells. Moreover, the administration of AKTin, an inhibitor of Akt, abolishes the protective effects of Serinc2 overexpression against inflammation and apoptosis. Our findings demonstrate a protective role of Serinc2 in the lung through activating the Akt pathway, and provide novel insight into the pathogenesis of sepsis-induced ALI.
期刊：
CELL DEATH & DISEASE,2022年13(9):756 ISSN：2041-4889
通讯作者：
Lu, Y.;Yu, X.-Q.
作者机构：
[Huang, Bo; Zhao, Ting; Ran, Mao-Jiu; Duan, Xin; Wang, Yu-Feng] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.;[Yu, Xiao-Qiang; Lu, Yuzhen; Xiao, Yanhong] South China Normal Univ, Inst Insect Sci & Technol, Guangdong Prov Key Lab Insect Dev Biol & Appl Tec, Guangzhou Key Lab Insect Dev Regulat & Applicat R, Guangzhou, Peoples R China.
通讯机构：
[Lu, Yuzhen; Yu, Xiao-Qiang] G;Guangdong Provincial Key Laboratory of Insect Developmental Biology and Applied Technology, Guangzhou Key Laboratory of Insect Development Regulation and Application Research, Institute of Insect Science and Technology, South China Normal University, Guangzhou, PR China
摘要：
In Drosophila ovary, niche is composed of somatic cells, including terminal filament cells (TFCs), cap cells (CCs) and escort cells (ECs), which provide extrinsic signals to maintain stem cell renewal or initiate cell differentiation. Niche establishment begins in larval stages when terminal filaments (TFs) are formed, but the underlying mechanism for the development of TFs remains largely unknown. Here we report that transcription factor longitudinals lacking (Lola) is essential for ovary morphogenesis. We showed that Lola protein was expressed abundantly in TFCs and CCs, although also in other cells, and lola was required for the establishment of niche during larval stage. Importantly, we found that knockdown expression of lola induced apoptosis in adult ovary, and that lola affected adult ovary morphogenesis by suppressing expression of Regulator of cullins 1b (Roc1b), an apoptosis-related gene that regulates caspase activation during spermatogenesis. These findings significantly expand our understanding of the mechanisms controlling niche establishment and adult oogenesis in Drosophila.
期刊：
Applied and Environmental Microbiology,2022年88(7):e0250521 ISSN：0099-2240
通讯作者：
Xiao, YT;Liu, KY
作者机构：
[Xiao, Yutao; Cheng, Ying; Liao, Chongyu; Jin, Minghui] Chinese Acad Agr Sci, Agr Genom Inst Shenzhen, Shenzhen Branch,Minist Agr, Guangdong Lab Lingnan Modern Agr,Genome Anal Lab, Shenzhen, Peoples R China.;[Liu, Kaiyu; Yang, Yongbo] Cent China Normal Univ, Coll Life Sci, Wuhan, Peoples R China.;[Soberon, Mario; Bravo, Alejandra] Univ Nacl Autonoma Mexico, Inst Biotecnol, Cuernavaca, Morelos, Mexico.
通讯机构：
[Xiao, YT ; Liu, KY ] C;Chinese Acad Agr Sci, Agr Genom Inst Shenzhen, Shenzhen Branch,Minist Agr, Guangdong Lab Lingnan Modern Agr,Genome Anal Lab, Shenzhen, Peoples R China.;Cent China Normal Univ, Coll Life Sci, Wuhan, Peoples R China.
作者机构：
[Zhang, Mengmeng; Guo, Xinghua; Zhen, Xuechu; Xu, Guoqiang; Ramprasad, Jurupula; Liu, Yanli; Ji, Xingyue] Soochow Univ, Jiangsu Key Lab Neuropsychiat Dis, Suzhou, Jiangsu, Peoples R China.;[Zhang, Mengmeng; Guo, Xinghua; Zhen, Xuechu; Xu, Guoqiang; Ramprasad, Jurupula; Liu, Yanli; Ji, Xingyue] Soochow Univ, Coll Pharmaceut Sci, Suzhou, Jiangsu, Peoples R China.;[Li, Weiguo; Min, Jinrong; Liu, Yanli] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Hubei, Peoples R China.;[Loppnau, Peter; Qin, Su; Li, Weiguo; Iqbal, Aman; Min, Jinrong; Brown, Peter J.; Liu, Yanli] Univ Toronto, Struct Genom Consortium, Toronto, ON, Canada.;[Zhou, Mengqi; Ni, Zuyao; Zhao, Dorothy Yanling; Greenblatt, Jack F.] Univ Toronto, Donnelly Ctr, Toronto, ON, Canada.
通讯机构：
[Liu, Yanli] J;[Min, Jinrong] H;Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, China<&wdkj&>Structural Genomics Consortium, University of Toronto, Toronto, Canada<&wdkj&>Department of Physiology, University of Toronto, Toronto, Canada<&wdkj&>Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, China<&wdkj&>Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, China<&wdkj&>Structural Genomics Consortium, University of Toronto, Toronto, Canada
摘要：
Survival of motor neuron (SMN) functions in diverse biological pathways via recognition of symmetric dimethylarginine (Rme2s) on proteins by its Tudor domain, and deficiency of SMN leads to spinal muscular atrophy. Here we report a potent and selective antagonist with a 4-iminopyridine scaffold targeting the Tudor domain of SMN. Our structural and mutagenesis studies indicate that both the aromatic ring and imino groups of compound 1 contribute to its selective binding to SMN. Various on-target engagement assays support that compound 1 specifically recognizes SMN in a cellular context and prevents the interaction of SMN with the R1810me2s of RNA polymerase II subunit POLR2A, resulting in transcription termination and R-loop accumulation mimicking SMN depletion. Thus, in addition to the antisense, RNAi and CRISPR/Cas9 techniques, potent SMN antagonists could be used as an efficient tool to understand the biological functions of SMN. The SMN protein recognizes symmetric dimethylarginine by its Tudor domain, and SMN deficiency leads to spinal muscular atrophy. Here, Liu et al. discover a small molecule that binds to the SMN Tudor domain and disrupts the interaction between SMN and RNA Polymerase II.
摘要：
Activating transcription factor 5 (Atf5) is a member of the ATF/CREB family of transcription factors and involved in diverse cellular functions and diseases in mammals. However, the function of atf5 remains largely unknown in fish. Here, we report the expression pattern and function of duplicated atf5 genes in zebrafish. The results showed that the gene structures of zebrafish atf5a and atf5b were similar to their mammalian orthologs. Zebrafish Atf5a and Atf5b shared an amino acid sequence identity of 40.7%. Zebrafish atf5a and atf5b had maternal origin with dynamic expression during embryonic development. Zebrafish atf5a mRNA is mainly enriched in olfactory epithelium, midbrain, and hindbrain, while zebrafish atf5b mRNA is mainly detected in midbrain, hindbrain, and liver during embryogenesis. The results of acute hypoxia experiment showed that atf5a mRNA was significantly upregulated in the brain, liver, and muscle, while atf5b mRNA was just increased significantly in the brain. Functional analysis showed that knockdown of atf5a affects the development of the ciliated neurons in zebrafish embryos. The effect was enhanced when atf5a MO was co-injected with atf5b MO. The development of ciliated neurons in zebrafish embryos was not affected by injection of atf5b MO alone. atf5a knockdown also affects the development of early-born olfactory neurons. The effects caused by atf5a knockdown could be rescued by atf5b mRNA. These results suggest that the duplicated atf5 genes may have evolved divergently and play redundant biological roles in the development of olfactory sensory neurons in zebrafish.
The expression patterns of zebrafish atf5a and atf5b are different but overlap in some regions during embryogenesis and in adult tissues. Zebrafish atf5a and atf5b genes may have evolved divergently and play redundant biological roles in olfactory sensory neurons development.
作者机构：
[Jiang, Yao; Liao, Xiaomei; Liu, Yabo; Liu, Qianhui; Mei, Mengjie; Wang, Shaohui] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.;[Liao, Xiaomei; Sun, Hongwei] Cent China Normal Univ, Coll Chem, Inst Environm & Appl Chem, Key Lab Pesticide & Chem Biol,Minist Educ, Wuhan 430079, Peoples R China.
通讯机构：
[Liao, Xiaomei] C;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.;Cent China Normal Univ, Coll Chem, Inst Environm & Appl Chem, Key Lab Pesticide & Chem Biol,Minist Educ, Wuhan 430079, Peoples R China.
关键词：
Ferroptosis;Glycogen synthase kinase-3β;Tau;Ubiquitin proteasome system
摘要：
Ferroptosis is a form of regulated cell death resulting from iron accumulation and lipid peroxidation. Iron dyshomeostasis and peroxidation damage of neurons in some particular brain regions are closely related to a wide range of neurodegenerative diseases known as "tauopathies," in which intracellular aggregation of microtubule-associated protein tau is the common neuropathological feature. However, the relationship between ferroptosis and tau aggregation is not well understood. The current study demonstrates that erastin-induced ferroptosis can promote tau hyperphosphorylation and aggregation in mouse neuroblastoma cells (N2a cells). Moreover, ferroptosis inhibitor ferrostatin-1 can alleviate tau aggregation effectively. In-depth mechanism research indicates that activated glycogen synthase kinase-3β (GSK-3β) is responsible for the abnormal hyperphosphorylation of tau. More importantly, proteasome inhibition can exacerbate tau degradation obstacle and accelerate tau aggregation in the process of ferroptosis. Our results indicate that ferroptosis can lead to abnormal aggregation of tau protein and might be a promising therapeutic target of tauopathies.
作者机构：
[Wang, Zhenhui; Zhang, Jian; Wang, Ningning] Jilin Agr Univ, Fac Agron, Changchun 131018, Peoples R China.;[Xun, Hongwei; Li, Guo; Wang, Ningning; Yu, Yanan; Zhang, Zhibin; Liu, Bao; Zhang, Di] Northeast Normal Univ, Minist Educ MOE, Key Lab Mol Epigenet, Changchun 130024, Peoples R China.;[Zhang, Di] Cent China Normal Univ, Sch Life Sci, Wuhan 430079, Peoples R China.;[Zhang, Jian] Univ British Columbia Okanagan, Dept Biol, Kelowna, BC V1V 1V7, Canada.
通讯机构：
[Jian Zhang] F;[Bao Liu] A;Faculty of Agronomy, Jilin Agricultural University, Changchun 131018, China<&wdkj&>Authors to whom correspondence should be addressed.<&wdkj&>Department of Biology, University of British Columbia Okanagan, Kelowna, BC V1V 1V7, Canada<&wdkj&>Authors to whom correspondence should be addressed.<&wdkj&>Key Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun 130024, China
期刊：
Journal of Biological Chemistry,2022年298(3):101623 ISSN：0021-9258
通讯作者：
Liu, Yanli;Min, Jinrong
作者机构：
[Yan, Xuemei; Yang, Yinxue; Liu, Yanli; Zhang, Mengmeng] Soochow Univ, Coll Pharmaceut Sci, Suzhou, Jiangsu, Peoples R China.;[Yang, Xiajie; Li, Fangzhou; Zhou, Mengqi; Min, Jinrong] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Hubei, Peoples R China.;[Wei, Zhengguo] Soochow Univ, Sch Biol & Basic Med Sci, Suzhou, Jiangsu, Peoples R China.;[Qin, Su] Southern Univ Sci & Technol, Life Sci Res Ctr, Shenzhen, Guangdong, Peoples R China.
通讯机构：
[Liu, Yanli] C;[Min, Jinrong] H;College of Pharmaceutical Sciences, Soochow University, Su Zhou, Jiangsu 215021, PR China. Electronic address:;Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, Hubei 430079, PR China. Electronic address:
摘要：
Arabidopsis LHP1 (LIKE HETEROCHROMATIN PROTEIN 1), a unique homolog of HP1 in Drosophila, plays important roles in plant development, growth, and architecture. In contrast to specific binding of the HP1 chromodomain to methylated H3K9 histone tails, the chromodomain of LHP1 has been shown to bind to both methylated H3K9 and H3K27 histone tails, and LHP1 carries out its function mainly via its interaction with these two epigenetic marks. However, the molecular mechanism for the recognition of methylated histone H3K9/27 by the LHP1 chromodomain is still unknown. In this study, we characterized the binding ability of LHP1 to histone H3K9 and H3K27 peptides and found that the chromodomain of LHP1 binds to histone H3K9me2/3 and H3K27me2/3 peptides with comparable affinities, although it exhibited no binding or weak binding to unmodified or monomethylated H3K9/K27 peptides. Our crystal structures of the LHP1 chromodomain in peptide-free and peptide-bound forms coupled with mutagenesis studies reveal that the chromodomain of LHP1 bears a slightly different chromodomain architecture and recognizes methylated H3K9 and H3K27 peptides via a hydrophobic clasp, similar to the chromodomains of human Polycomb proteins, which could not be explained only based on primary structure analysis. Our binding and structural studies of the LHP1 chromodomain illuminate a conserved ligand interaction mode between chromodomains of both animals and plants, and shed light on further functional study of the LHP1 protein.
作者机构：
[Jiang, Hai-Bo; Liu, Ling-Mei; Li, Ding-Lan; Deng, Bin] Cent China Normal Univ, Sch Life Sci, Wuhan 430079, Hubei, Peoples R China.;[Wang, Xin-Wei; Jiang, Hai-Bo; Liu, Ling-Mei] Southern Marine Sci & Engn Guangdong Lab Zhuhai, Zhuhai 519080, Guangdong, Peoples R China.;[Wang, Xin-Wei; Jiang, Hai-Bo] Ningbo Univ, Sch Marine Sci, Ningbo 315211, Zhejiang, Peoples R China.
通讯机构：
[Hai-Bo Jiang] S;School of Life Sciences, Central China Normal University, Wuhan, Hubei, 430079 China<&wdkj&>Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Zhuhai, Guangdong, 519080 China<&wdkj&>School of Marine Sciences, Ningbo University, Ningbo, Zhejiang, 315211 China
通讯机构：
[Hai-Feng Xu; Guo-Zheng Dai; Bao-Sheng Qiu] S;School of Life Sciences, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, Central China Normal University, Wuhan 430079, China
关键词：
desiccation tolerance;cyanobacteria;Nostoc;high light-inducible protein
作者机构：
[Huang, Shuang-Quan; Han, Wen-Long; Li, Deng-Fei] Cent China Normal Univ, Inst Evolut & Ecol, Sch Life Sci, Wuhan, Peoples R China.;[Renner, Susanne S.] Washington Univ, Dept Biol, St Louis, MO USA.
关键词：
berberine in pollen;ecology;male reproductive success;plant–insect interactions;pollen flow;snapping stamens;stimulated movement
摘要：
Animal-pollinated plants have to get pollen to a conspecific stigma while protecting it from getting eaten. Touch-sensitive stamens, which are found in hundreds of flowering plants, are thought to function in enhancing pollen export and reducing its loss, but experimental tests are scarce. Stamens of Berberis and Mahonia are inserted between paired nectar glands and when touched by an insect's tongue rapidly snap forward so that their valvate anthers press pollen on the insect's tongue or face. We immobilized the stamens in otherwise unmodified flowers and studied pollen transfer in the field and under enclosed conditions. On flowers with immobilized stamens, the most common bee visitor stayed up to 3.6× longer, yet removed 1.3× fewer pollen grains and deposited 2.1× fewer grains on stigmas per visit. Self-pollen from a single stamen hitting the stigma amounted to 6% of the grains received from single bee visits. Bees discarded pollen passively placed on their bodies, likely because of its berberine content; nectar has no berberine. Syrphid flies fed on both nectar and pollen, taking more when stamens were immobilized. Pollen-tracking experiments in two Berberis species showed that mobile-stamen-flowers donate pollen to many more recipients. These results demonstrate another mechanism by which plants simultaneously meter out their pollen and reduce pollen theft.
