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Hepatic steatosis is associated with dysregulated cholesterol metabolism and altered protein Acetylation dynamics in chickens

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Journal of Animal Science and Biotechnology 2024年第1期15卷 53-67页

作者： Xiaoli Guo Qianqian Zhou Jiaming Jin Fangren Lan Chaoliang Wen Junying Li Ning Yang Congjiao Sun National Engineering Laboratory for Animal Breeding and Key Laboratory of Animal Genetics Breeding and ReproductionMinistry of Agriculture and Rural AffairsChina Agricultural UniversityBeijing 100193China

Background Hepatic steatosis is a prevalent manifestation of fatty liver, that has detrimental effect on the health and productivity of laying hens, resulting in economic losses to the poultry industry. Here, we aimed to systematically investigate the genetic regulatory mechanisms of hepatic steatosis in laying hens.Methods Ninety individuals with the most prominent characteristics were selected from 686 laying hens according to the accumulation of lipid droplets in the liver, and were graded into three groups, including the control, mild hepatic steatosis and severe hepatic steatosis groups. A combination of transcriptome, proteome, acetylome and lipidome analyses, along with bioinformatics analysis were used to screen the key biological processes, modifications and lipids associated with hepatic steatosis.Results The rationality of the hepatic steatosis grouping was verified through liver biochemical assays and RNA-seq. Hepatic steatosis was characterized by increased lipid deposition and multiple metabolic abnormalities. Integration of proteome and acetylome revealed that differentially expressed proteins(DEPs) interacted with differentially acetylated proteins(DAPs) and were involved in maintaining the metabolic balance in the liver. Acetylation alterations mainly occurred in the progression from mild to severe hepatic steatosis, i.e., the enzymes in the fatty acid oxidation and bile acid synthesis pathways were significantly less acetylated in severe hepatic steatosis group than that in mild group(P Acetylation in hepatic steatosis and depict the ch

关键词： Acetylation Cholesterol metabolism Hepatic steatosis Laying hens Multiomics

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Histone deacetylase inhibitors inhibit cervical cancer growth through Parkin Acetylationmediated mitophagy

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Acta Pharmaceutica Sinica B 2022年第2期12卷 838-852页

作者： Xin Sun Yuhan Shu Guiqin Ye Caixia Wu Mengting Xu Ruilan Gao Dongsheng Huang Jianbin Zhang Department of Oncology Cancer Center of Zhejiang Provincial People’s HospitalAffiliated People’s HospitalHangzhou Medical CollegeHangzhou 310014China Clinical Research Institute Zhejiang Provincial People’s HospitalAffiliated People’s HospitalHangzhou Medical CollegeHangzhou 310014China Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province Hangzhou Medical CollegeHangzhou 310014China College of Biomedical Engineering&Instrument Science Zhejiang UniversityHangzhou 310028China Department of Hematology the First Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310006China

Parkin,an E3 ubiquitin ligase,plays a role in maintaining mitochondrial homeostasis through targeting damaged mitochondria for mitophagy.Accumulating evidence suggests that the Acetylation modification of the key mitophagy machinery influences mitophagy level,but the underlying mechanism is poorly understood.Here,our study demonstrated that inhibition of histone deacetylase(HDAC)by treatment of HDACis activates mitophagy through mediating Parkin Acetylation,leading to inhibition of cervical cancer cell proliferation.Bioinformatics analysis shows that Parkin expression is inversely correlated with HDAC2 expression in human cervical cancer,indicating the low Acetylation level of Parkin.Using mass spectrometry,Parkin is identified to interact with two upstream molecules,acetylase acetyl-Co A acetyltransferase 1(ACAT1)and deacetylase HDAC2.Under treatment of suberoylanilide hydroxamic acid(SAHA),Parkin is acetylated at lysine residues 129,220 and 349,located in different domains of Parkin protein.In in vitro experiments,combined mutation of Parkin largely attenuate the interaction of Parkin with PTEN induced putative kinase 1(PINK1)and the function of Parkin in mitophagy induction and tumor suppression.In tumor xenografts,the expression of mutant Parkin impairs the tumor suppressive effect of Parkin and decreases the anticancer activity of SAHA.Our results reveal an Acetylation-dependent regulatory mechanism governing Parkin in mitophagy and cervical carcinogenesis,which offers a new mitophagy modulation strategy for cancer therapy.

关键词： Parkin Mitophagy ACAT1 HDAC2 Acetylation Ubiquitination Tumor suppression Cervical cancer

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Regulation of jasmonate signaling by reversible Acetylation of TOPLESS in Arabidopsis

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Molecular Plant 2022年第8期15卷 1329-1346页

作者： Chunpeng An Lei Deng Huawei Zhai Yanrong You Fangming Wu Qingzhe Zhai Alain Goossens Chuanyou Li State Key Laboratory of Plant Genomics National Center for Plant Gene Research(Beijing)Institute of Genetics and Developmental BiologyInnovation Academy of Seed DesignChinese Academy of SciencesBeijing 100101China CAS Center for Excellence in Biotic Interactions University of Chinese Academy of SciencesBeijing 100049China State Key Laboratory of Crop Biology College of Horticulture Science and EngineeringShandong Agricultural UniversityTai'an 271018China Department of Plant Biotechnology and Bioinformatics Ghent UniversityTechnologiepark 719052 GhentBelgium VIB Center for Plant Systems Biology Technologiepark 719052 GhentBelgium

The plant hormone jasmonate(JA)regulates plant immunity and adaptive growth by orchestrating a genome-wide transcriptional program.Key regulators of JA-responsive gene expression include the master transcription factor MYc2,which is repressed by the conserved Groucho/Tup1-like corepressor TOPLESS(TPL)in the resting state.However,the mechanisms underlying TPL-mediated transcriptional repression of MYc2 activity and hormone-dependent switching between repression and de-repression remainenigmatic.Here,we report the regulation of TPLactivity and JAsignaling byreversibleAcetylation of TPL.We found that the histone acetyltransferase GCN5 could mediate TPL Acetylation,which enhances its interaction with the NOVEL-INTERACTOR-OF-JAZ(NINJA)adaptor and promotes its recruitment to MYc2 target promoters,facilitating transcriptional repression.Conversely,TPL deAcetylation by the histonedeacetylase HDA6 weakens TPL-NINJA interaction and inhibitsTPL recruitmentto MYC2 target promoters,facilitating transcriptional activation.In the resting state,the opposing activities of GCN5 and HDA6 maintain TPL Acetylation homeostasis,promoting transcriptional repression activity of TPL.In response to JA elicitation,HDA6 expression is transiently induced,resulted in decreased TPL Acetylation and repressor activity,thereby transcriptional activation of MYC2 target genes.Thus,the GCN5-TPL-HDA6 module main tains the homeostasis of acetylated TPL,thereby determining the transcriptional state of JA-responsive genes.Our findings uncovered a mechanism by which the TPL corepressor activity in JA signaling is activelytuned inarapidandreversiblemanner.

关键词： jasmonate signaling transcriptional repression TOPLESS corepressor GCN5 HDA6 Acetylation

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Alternatively mechanistic insights into Acetylation in p53-mediated transcriptional regulation of cancer cell-intrinsic PD-1

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Fundamental Research 2023年第4期3卷 647-654页

作者： Jia Wen Han Yao Zhijie Cao Donglai Wang State Key Laboratory of Medical Molecular Biology&Department of Medical Genetics Institute of Basic Medical Sciences&School of Basic MedicineChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100005China

Since the recent discovery of cancer cell-intrinsic programmed cell death protein-1(PD-1),the mechanisms that manipulate PD-1 functions in tumor development beyond its immune checkpoint roles have become attractive research topics in oncology.Our previous study validated that PD-1 exists in lung cancer cells and is directly transactivated by p53 in a DNA-binding domain(DBD)Acetylation-dependent manner.Here,we report that the carboxyl-terminal domain(CTD)of p53 likewise participates in PD-1 transcriptional regulation in cancer cells under different regulatory mechanisms.By mutating the lysine residues within the CTD to mimic either Acetylationdeficient or fully acetylated status,we proved that acetylated CTD dramatically impeded p53-mediated transactivation of PD-1.Furthermore,we identified bromodomain-containing protein 4(BRD4)as a transcriptional coactivator of p53 that facilitates p53-mediated PD-1 transcription.Mechanistically,BRD4 specifically bound to the unacetylated CTD of p53,while CTD Acetylation almost completely destroyed the BRD4-p53 interaction and thus led to compromised PD-1 expression.Collectively,this study unveils an alternative mechanism of p53 Acetylation-directed PD-1 transcriptional regulation,which would broaden our current understanding of the molecular regulatory network of cancer cell-intrinsic PD-1.

关键词： p53 Acetylation PD-1 BRD4 Carboxyl-terminal Domain(CTD)

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CBP-mediated Slug Acetylation stabilizes Slug and promotes EMT and migration of breast cancer cells

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Science China(Life Sciences) 2021年第4期64卷 563-574页

作者： Xiaoyan Dai Yanli Xin Weizhi Xu Xinxia Tian Xiaofan Wei Hongquan Zhang Deparment of Human Anatomy Histologyand EmbrpologyKey Laboratory of Carcinogenesis and Translational Research(Minsiry of Education)and State Key Laboralory of Natural and Biomimetic DrugsSchool of Basic Medical SciencesPeking University Health Science CenterBejing 100191China Deparment of Pathology School of Basic Medical SciencesPeking University Heath Science CenterBejing 100191China

Slug,a member of the Snail family of transcriptional repressors,plays a key role in cancer progression,cellular plasticity,and epithelial to mesenchymal transition(EMT).Slug is a fast-turnover protein and its stability is controlled by post-translational modifications.Here,we identified that Slug is acetylated by acetyltransferase CREB-binding protein(CBP)in breast cancer cells.CBP directly interacts with the C-terminal domain of Slug through its catalytic histone acetyltransferase(HAT)domain,leading to Acetylation of Slug at lysines 166 and 211.Analysis with Acetylation-specific antibodies revealed that Slug is highly acetylated in metastatic breast cancer cells.Notably,Slug Acetylation,mediated by CBP at lysines 166 and 211,doubles its halflife and increases its stability.Further,acetylated Slug downregulates the expression of E-cadherin,the epithelial marker,and upregulates the expression of N-cadherin and vimentin,thereby promoting breast cancer cell migration.In conclusion,the present study demonstrates that CBP-mediated Slug Acetylation increases its stability,promoting EMT and migration of breast cancer cells.

关键词： Slug Acetylation breast cancer EMT

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Acetylation of ezrin regulates membrane–cytoskeleton interaction underlying CCL18-elicited cell migration

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Journal of Molecular Cell Biology 2020年第6期12卷 424-437页

作者： Xiaoyu Song Wanjuan Wang Haowei Wang Xiao Yuan Fengrui Yang Lingli Zhao McKay Mullen Shihao Du Najdat Zohbi Saravanakumar Muthusamy Yalei Cao Jiying Jiang Peng Xia Ping He Mingrui Ding Nerimah Emmett Mingming Ma Quan Wu Hadiyah-Nicole Green Xia Ding Dongmei Wang Fengsong Wang Xing Liu School of Traditional Medicine Beijing University of Chinese MedicineBeijingChina MOE Key Laboratory for Membraneless Organelles&Cellular Dynamics Hefei National Center for Physical Sciences at the MicroscaleHefeiChina Morehouse School of Medicine Keck Center for Organoids PlasticityAtlantaGAUSA Optics and Optical Engineering University of Science and Technology of ChinaHefeiChina School of Life Science Anhui Medical UniversityHefeiChina

Ezrin,a membrane–cytoskeleton linker protein,plays an essential role in cell polarity establishment,cell migration,and division.Recent studies show that ezrin phosphorylation regulates breast cancer metastasis by promoting cancer cell survivor and promotes intrahepatic metastasis via cell migration.However,it was less characterized whether there are additional post-translational modifications and/or post-translational crosstalks on ezrin underlying context-dependent breast cancer cell migration and invasion.Here we show that ezrin is acetylated by p300/CBP-associated factor(PCAF)in breast cancer cells in response to CCL18 stimulation.Ezrin physically interacts with PCAF and is a cognate substrate of PCAF.The Acetylation site of ezrin was mapped by mass spectrometric analyses,and dynamic Acetylation of ezrin is essential for CCL18-induced breast cancer cell migration and invasion.Mechanistically,the Acetylation reduced the lipid-binding activity of ezrin to ensure a robust and dynamic cycling between the plasma membrane and cytosol in response to CCL18 stimulation.Biochemical analyses show that ezrin Acetylation prevents the phosphorylation of Thr567.Using atomic force microscopic measurements,our study revealed that Acetylation of ezrin induced its unfolding into a dominant structure,which prevents ezrin phosphorylation at Thr567.Thus,these results present a previously undefined mechanism by which CCL18-elicited crosstalks between the Acetylation and phosphorylation on ezrin control breast cancer cell migration and invasion.This suggests that targeting PCAF signaling could be a potential therapeutic strategy for combating hyperactive ezrin-driven cancer progression.

关键词： ezrin Acetylation phosphorylation actin cell migration

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Icariin Improves Cognitive Impairment after Traumatic Brain Injury by Enhancing Hippocampal Acetylation

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Chinese Journal of Integrative Medicine 2018年第5期24卷 366-371页

作者： ZHANG Zi-gang WANG Xin ZAI Jin-hai SUN Cai-hua YAN Bing-chun Department of Neurology Jiangyin Hospital of Traditional Chinese Medicine Jiangyin Jiangsu Province (214400) China Department of Pathogeny Microbiology Jiangsu University Zhenjiang Jiangsu Province (212013) China Department of Rehabilitation Northern Jiangsu People's Hospital Yangzhou Jiangsu Province (225001) China Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases Yangzhou Jiangsu Province (225001) China Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses Yangzhou Jiangsu Province (225009) China

Objective: To examine the effect of icariin(ICA) on the cognitive impairment induced by traumatic brain injury(TBI) in mice and the underlying mechanisms related to changes in hippocampal Acetylation level. Methods: The modified free-fall method was used to establish the TBI mouse model. Mice with post-TBI cognitive impairment were randomly divided into 3 groups using the randomised block method(n=7): TBI(vehicle-treated), low-dose(75 mg/kg) and high-dose(150 mg/kg) of ICA groups. An additional sham-operated group(vehicle-treated) was employed. The vehicle or ICA was administrated by gavage for 28 consecutive days. The Morris water maze(MWM) test was conducted. Acetylcholine(ACh) content, m RNA and protein levels of choline acetyltransferase(Ch AT), and protein levels of acetylated H3(Ac-H3) and Ac-H4 were detected in the hippocampus. Results: Compared with the sham-operated group, the MWM performance, hippocampal ACh content, m RNA and protein levels of Ch AT, and protein levels of Ac-H3 and Ac-H4 were significantly decreased in the TBI group(PAcetylation, which improved hippocampal cholinergic function and ultimately improved cognition.

关键词： icariin traumatic brain injury cognitive impairment Acetylation hippocampus

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Acetylation of H3K4,H3K9,and H3K27 mediated by p300 regulates the expression of GATA4 in cardiocytes

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Genes & Diseases 2019年第3期6卷 318-325页

作者： Wei Zhou Dagui Jiang Jie Tian Lingjuan Liu Tiewei Lu Xupei Huang Huichao Sun Heart Centre Children’s Hospital of Chongqing Medical UniversityMinistry of Education Key Laboratory of Child Development and DisordersChongqing400014China China International Science and Technology Cooperation Base of Child Development and Critical Disorders Chongqing400014China Chongqing Key Laboratory of Pediatrics Chongqing400014China Department of Biomedical Science Charlie E.Schmidt College of MedicineFlorida Atlantic UniversityBoca RatonFLUSA Heart Centre Children’s Hospital of Chongqing Medical UniversityChongqing400014China

GATA4 is a particularly important cardiogenic transcription factor and serves as a potent driver of cardiogenesis.Recent progress in the field has made it clear that histone Acetylation can influence gene expression through changing the structure of chromatin.Our previous research had revealed that hypo-Acetylation could repress gata4 expression in cardiocytes,however the underlying mechanism by which this occurred was still unclear.To reveal the mechanism of histone Acetylation involved in the regulation of gata4 transcription,we concentrated on P300,one of the important histone acetyltransferase associated with cardiogenesis.We found that P300 participated in gata4 expression through regulating histone Acetylation in embryonic mouse hearts.RNAi-mediated downregulation of P300 modulated the global Acetylation of H3 and the Acetylation of H3K4,H3K9,and H3K27 in gata4 and Tbx5 promoters.Interestingly,there was an obvious inhibition of gata4 transcription,whereas Tbx5 was not influenced.Furthermore,SGC-CBP30,the selective inhibitor of the bromodomain in CBP/P300,downregulated gata4 transcription by repressing the Acetylation of H3K4,H3K9,and H3K27 in the gata4 promoters.Taken together,our results identified that Acetylation of H3K4,H3K9,and H3K27 mediated by P300 plays an important role in regulation of gata4 expression in cardiogenesis.

关键词： gata4 P300 Acetylation H3K4ac H3K9ac H3K27ac

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Sublytic C5b-9 triggers glomerular mesangial cell apoptosis in rat Thy-1 nephritis via Gadd45 activation mediated by Egr-1 and p300-dependent ATF3 Acetylation

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Journal of Molecular Cell Biology 2016年第6期8卷 477-491页

作者： Fengxia He Mengya Zhou Tianyi Yu Dan Zhao Jing Zhang Wen Qiu Yanlai Lu Yu Liu Lulu Wang Yingwei Wang Department of Immunology Nanjing Medical UniversityNanjing 210029China

The apoptosis of glomerular mesangial cells(GMCs)is considered to be an important contributor to the initiation and development of rat Thy-1 nephritis(Thy-1N)and is accompanied by sublytic C5b-9 deposition.However,the mechanism by which sublytic C5b-9 triggers GMC apoptosis has not been elucidated.In this study,functional and histological examinations were performed on GMCs treated with sublytic C5b-9(in vitro)and renal tissues of Thy-1N rats(in vivo).The in vitro studies found that sublytic C5b-9 could trigger GMC apoptosis through upregulating Egr-1,ATF3,and Gadd45 expression.Egr-1-mediated post-transcriptional modulation of ATF3,Egr-1/ATF3-enhanced Gadd45 promoter activity,and p300-mediated ATF3 Acetylation were all involved in GMC apoptosis.More importantly,the effective binding elements for Egr-1 and ATF3 to Gadd45β/γpromoters and the ATF3 Acetylation site were identified.In vivo,silencing renal p300,Egr-1,ATF3,and Gadd45β/γsignificantly decreased GMC apoptosis,secondary GMC proliferation,and urinary protein secretion in Thy-1N rats.Together,these findings implicate that sublytic C5b-9-induced activation of Egr-1/p300–ATF3/Gadd45 axis plays a critical role in GMC apoptosis in Thy-1N rats.

关键词： glomerular mesangial cells sublytic C5b-9 Thy-1 nephritis transcription factor Acetylation apoptosis

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Acetylation of Nup62 by TIP60 ensures accurate chromosome segregation in mitosis

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Journal of Molecular Cell Biology 2022年第8期14卷 53-66页

作者： Hameed Akbar Jun Cao Dongmei Wang Xiao Yuan Manjuan Zhang Saravanakumar Muthusamy Xiaoyu Song Xu Liu Felix Aikhionbare Xuebiao Yao Xinjiao Gao Xing Liu MOE Key Laboratory for Cellular Dynamics and School of Life Sciences University of Science and Technology of ChinaHefei 230027China CAS Center for Excellence in Molecular and Cell Sciences Anhui Key Laboratory for Cellular Dynamics and Chemical BiologyHefei 230027China Morehouse School of Medicine AtlantaGA 30310USA

Stable transmission of genetic information during cell division requires faithful mitotic spindle assembly and chromosome segregation.In eukaryotic cells,nuclear envelope breakdown(NEBD)is required for proper chromosome segregation.Although a list of mitotic kinases has been implicated in NEBD,how they coordinate their activity to dissolve the nuclear envelope and protein machinery such as nuclear pore complexes was unclear.Here,we identified a regulatory mechanism in which Nup62 is acetylated by TIP60 in human cell division.Nup62 is a novel substrate of TIP60,and the Acetylation of Lys432 by TIP60 dissolves nucleoporin Nup62-Nup58-Nup54 complex during entry into mitosis.Importantly,this Acetylation-elicited remodeling of nucleoporin complex promotes the distribution of Nup62 to the mitotic spindle,which is indispensable for orchestrating correct spindle orientation.Moreover,suppression of Nup62 perturbs accurate chromosome segregation during mitosis.These results establish a previously uncharacterized regulatory mechanism in which TIP60-elicited nucleoporin dynamics promotes chromosome segregation in mitosis.

关键词： mitosis spindle Nup62 TIP60 Acetylation

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