Recent Evolution of Bacterial Pathogens: Tne Gall-Forming Pantoea agglomerans Case

被引:80
作者
Barash, Isaac [1 ]
Manulis-Sasson, Shulamit [2 ]
机构
[1] Tel Aviv Univ, Fac Life Sci, Dept Plant Sci, IL-61390 Tel Aviv, Israel
[2] ARO, Volcani Ctr, Dept Plant Pathol & Weed Res, IL-50250 Bet Dagan, Israel
基金
以色列科学基金会;
关键词
hrp/hrc gene cluster; auxin; cytokinins; pathogenicity island; host specificity; quorum sensing regulation; ERWINIA-HERBICOLA PV; III SECRETION SYSTEM; INDOLE-3-ACETIC-ACID BIOSYNTHETIC PATHWAYS; PHYTOPATHOGEN RHODOCOCCUS-FASCIANS; SYRINGAE SUBSP-SAVASTANOI; EFFECTOR PROTEINS; CYTOKININ BIOSYNTHESIS; HOST-SPECIFICITY; ENTEROBACTER-AGGLOMERANS; PATHOADAPTIVE MUTATIONS;
D O I
10.1146/annurev-phyto-080508-081803
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Pantoea agglomerans, a widespread epiphyte and commensal bacterium, has evolved into an Hrp-dependent and host-specific tumorigenic pathogen by acquiring a plasmid containing a pathogenicity island (PAI). The PAI was evolved on an iteron plasmid of the IncN family, which is distributed among genetically diverse populations of P. agglomerans. The structure of the PAI supports the premise of a recently evolved pathogen. This review offers insight into a unique model for emergence of new bacterial pathogens. It illustrates how horizontal gene transfer was the major driving force in the creation of the PAI, although a pathoadaptive mechanism might also be involved. It describes the crucial function of plant-produced indole-3-acetic acid (IAA) and cytokinines (CK) in gall initiation as opposed to the significant but secondary role of pathogensecreted phytohormones. It also unveils the role of type III effectors in determination of host specificity and evolution of the pathogen into pathovars. Finally, it describes how interactions between the quorum sensing system, hrp regulatory genes, and bacterially secreted IAA or CKs affect gall formation and epiphytic fitness.
引用
收藏
页码:133 / 152
页数:20
相关论文
共 114 条
[1]  
Abeles F. B., 1992, ETHYLENE PLANT BIOL
[2]   Type III secretion system effector proteins: Double agents in bacterial disease and plant defense [J].
Alfano, JR ;
Collmer, A .
ANNUAL REVIEW OF PHYTOPATHOLOGY, 2004, 42 :385-414
[3]  
Arnold DL, 2003, MOL PLANT PATHOL, V4, P407, DOI [10.1046/j.1364-3703.2003.00187.x, 10.1046/J.1364-3703.2003.00187.X]
[4]   Integration of two models or dominance of one? [J].
Baranowski, T .
JOURNAL OF HEALTH PSYCHOLOGY, 2005, 10 (01) :19-21
[5]   Virulence mechanisms and host specificity of gall-forming Pantoea agglomerans [J].
Barash, Isaac ;
Manulis-Sasson, Shulamit .
TRENDS IN MICROBIOLOGY, 2007, 15 (12) :538-545
[6]   SUBJECTIVE SYNONYMY OF ERWINIA-HERBICOLA, ERWINIA-MILLETIAE, AND ENTEROBACTER-AGGLOMERANS AND REDEFINITION OF THE TAXON BY GENOTYPIC AND PHENOTYPIC DATA [J].
BEJI, A ;
MERGAERT, J ;
GAVINI, F ;
IZARD, D ;
KERSTERS, K ;
LECLERC, H ;
DELEY, J .
INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY, 1988, 38 (01) :77-88
[7]   Anatomy of cranberry stem gall and localization of bacteria in galls [J].
Best, VM ;
Vasanthakumar, A ;
McManus, PS .
PHYTOPATHOLOGY, 2004, 94 (11) :1172-1177
[8]  
Binns A. N., 1998, The Rhizobiaceae: molecular biology of model plant-associated bacteria., P251
[9]   VIRULENCE GENES ARE CARRIED BY A MEGAPLASMID OF THE PLANT PATHOGEN PSEUDOMONAS-SOLANACEARUM [J].
BOUCHER, C ;
MARTINEL, A ;
BARBERIS, P ;
ALLOING, G ;
ZISCHEK, C .
MOLECULAR & GENERAL GENETICS, 1986, 205 (02) :270-275
[10]  
BRADY CL, 2006, P INT C PLANT PATH B, P23