tRNA修饰酶GidA家族蛋白研究进展
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摘要
葡萄糖抑制的分裂蛋白A(GidA)是一种tRNA修饰酶,在原核生物和真核生物中都非常保守,参与对tRNA的摇摆碱基尿嘧啶进行修饰,然后解码以腺嘌呤或鸟嘌呤结尾的密码子。GidA的这种修饰作用对蛋白质的精确解码和高效翻译至关重要。近年来,对GidA在细胞中的功能研究较多,发现GidA不仅调控细胞的形态还与致病性密切相关,而该蛋白在人类中的同源蛋白MTO1的突变与心肌病变、呼吸障碍、癫痫等多种疾病相关。作者查阅了相关资料,对GidA功能与结构的研究进行综述,以期为了解病原菌的致病机制与人类相关疾病的发病机理提供参考。
GidA-like proteins are tRNA modification enzyme,widely distributed in nature and conserved among bacteria and Eukarya.GidA involves in the addition of the carboxymethylaminomethyl(cmnm)group in position 5 of the U34 of tRNAs that read codons ending with A or G.This modification at the wobble position of the anticodon contributes to the accuracy and efficiency of protein synthesis.Recent years,more and more research focused on cell function of GidA.GidA not only regulates morphology but also pathogenicity in several bacteria.Human mutations of the gidAhomologous gene,MTO1,are often associated with hypertrophic cardiomyopathy,respiratory defect,seizures.Through consulting literature materials,we summarized the function and structure of GidA.We hope this review about GidA-like proteins could help in understanding the pathogenesis of pathogenic bacteria and related human diseases.
GidA-like proteins are tRNA modification enzyme,widely distributed in nature and conserved among bacteria and Eukarya.GidA involves in the addition of the carboxymethylaminomethyl(cmnm)group in position 5 of the U34 of tRNAs that read codons ending with A or G.This modification at the wobble position of the anticodon contributes to the accuracy and efficiency of protein synthesis.Recent years,more and more research focused on cell function of GidA.GidA not only regulates morphology but also pathogenicity in several bacteria.Human mutations of the gidAhomologous gene,MTO1,are often associated with hypertrophic cardiomyopathy,respiratory defect,seizures.Through consulting literature materials,we summarized the function and structure of GidA.We hope this review about GidA-like proteins could help in understanding the pathogenesis of pathogenic bacteria and related human diseases.
引文
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[2]Lence T,Akhtar J,Bayer M,et al.m6A modulates neuronal functions and sex determination in Drosophila[J].Nature,2016,540(7632):242-247.
[3]Manickam N,Joshi K,Bhatt M J,et al.Effects of tRNA modification on translational accuracy depend on intrinsic codon-anticodon strength[J].Nucleic Acids Res,2016(44):1871-1881.
[4]周觅,刘如娟,王恩多.tRNA转录后修饰的功能及其与人类疾病的关系[J].生命科学,2014,26(10):1032-1037.
[5]Yacoubi B,Bailly M,Crécy-Lagard V.Biosynthesis and function of posttranscriptional modifications of transfer RNAs[J].Annual Rev Gen,2012,46:69-95.
[6]Moukadiri I,Garzón J,Bj9rk R,et al.The output of the tRNA modification pathways controlled by the Escherichia coli MnmEG and MnmC enzymes depends on the growth conditions and the tRNAspecies[J].Nucleic Acids Res,2014,42:2602-2623.
[7]Tkenmez H,Xu H,Esberg A,et al.The role of wobble uridine modifications in+1translational frameshifting in eukaryotes[J].Nucleic Acids Res,2015,43(19):9489-9499.
[8]Shaheen R,Han L,Faqeih E,et al.A homozygous truncating mutation in PUS3expands the role of tRNA modification in normal cognition[J].Human Gen,2016,135:707-713.
[9]Roundtree A,Evans E,Pan T,et al.Dynamic RNA modifications in gene expression regulation[J].Cell,2017,169:1187-1200.
[10]Boutoual R,Meseguer S,Villarroya M,et al.Defects in the mitochondrial-tRNA modification enzymes MTO1and GT-PBP3promote different metabolic reprogramming through a HIF-PPARγ-UCP2-AMPK axis[J].Sci Report,2018,18,8(1):1163.
[11]Meyenburg K,Jorgensen B,Nielsen J,et al.Promoters of the atp operon coding for the membrane-bound ATP synthase of Escherichia coli mapped by Tn10insertion mutations[J].Mol Gen Genetics,1982,188:240-248.
[12]Gao T,Tan M,Liu W,et al.GidA,a tRNA Modification enzyme,contributes to the growth,and virulence of Streptococcus suis serotype 2[J].Front Cell Infect Microbiol,2016,6:44.
[13]Shippy C,Heintz A,Albrecht M,et al.Deletion of glucose-inhibited division(gidA)gene alters the morphological and replication characteristics of Salmonella enterica serovar typhimurium[J].Arch Microbiol,2012,194:405-412.
[14]Li D,Shibata Y,Takeshita T,et al.A novel gene involved in the survival of Streptococcus mutans under stress conditions[J].Appl Environ Microbiol,2013,80:97-103.
[15]Lies M,Visser J,Joshi C,et al.MioC and GidA proteins promote cell division in E.coli[J].Front Microbiol,2015,6:516.
[16]Yu L,Kim S.mRNA context dependent regulation of cytotoxic necrotizing factor 1translation by GidA,a tRNA modification enzyme in Escherichia coli[J].Gene,2012,491:116-22.
[17]Shippy C,Eakley M,Lauhon T,et al.Virulence characteristics of Salmonellafollowing deletion of genes encoding the tRNAmodification enzymes GidA and MnmE[J].Microb Pathog,2013,57,1-9.
[18]Shippy C,Eakley M,Bochsler N,et al.Biological and virulence characteristics of Salmonella enterica serovar typhimuriumfollowing deletion of glucose-inhibited division(gidA)gene[J].Microbial Pathog,2011,50,303-313.
[19]Becker L,Kling E,Schiller E,et al.MTO1-deficient mouse model mirrors the human phenotype showing complex I defect and cardiomyopathy[J].PLoS One,2014,9(12):e114918.
[20]Ghezzi D,Baruffini E,Haack B,et al.Mutations of themitochondrial-tRNA modifier MTO1cause hypertrophic cardiomyopathy and lactic acidosis[J].Am J Human Genetics,2012,90:1079-1087.
[21]Baruffini E,Dallabona C,Invernizzi F,et al.MTO1mutations are associated with hypertrophic cardiomyopathy and lactic acidosis and cause respiratory chain deficiency in humans and yeast[J].Human Mutation,2013,34(11):1501-9.
[22]Boutoual R,Meseguer S,Villarroya M,et al.Defects in the mitochondrial-tRNA modification enzymes MTO1and GTPBP3promote different metabolic reprogramming through a HIF-PPARγ-UCP2-AMPK axis[J].Sci Reports,2018,8:1163.