Selection footprint in the FimH adhesin shows pathoadaptive niche differentiation in Escherichia coli

被引:79
作者
Sokurenko, EV [1 ]
Feldgarden, M
Trintchina, E
Weissman, SJ
Avagyan, S
Chattopadhyay, S
Johnson, JR
Dykhuizen, DE
机构
[1] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA
[2] Univ Minnesota, Sch Med, Dept Med, Minneapolis, MN 55455 USA
[3] Univ Minnesota, Sch Med, Vet Adm Med Ctr, Minneapolis, MN 55455 USA
[4] SUNY Stony Brook, Dept Ecol & Evolut, Stony Brook, NY 11794 USA
关键词
bacterial pathogens; niche differentiation; selection footprint;
D O I
10.1093/molbev/msh136
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Spread of biological species from primary into novel habitats leads to within-species adaptive niche differentiation and is commonly driven by acquisition of point mutations in individual genes that increase fitness in the alternative environment. However, finding footprints of adaptive niche differentiation in specific genes remains a challenge. Here we describe a novel method to analyze the footprint of pathogenicity-adaptive, or pathoadaptive, mutations in the Escherichia coli gene encoding FimH-the major, mannose-sensitive adhesin. Analysis of distribution of mutations across the nodes and branches of the FimH phylogenetic network shows (1) zonal separation of evolutionary primary structural variants of FimH and recently derived ones, (2) dramatic differences in the ratio of synonymous and nonsynonymous changes between nodes from different zones, (3) evidence for replacement hot-spots in the FimH protein, (4) differential zonal distribution of FimH variants from commensal and uropathogenic E. coli, and (5) pathoadaptive functional changes in FimH brought by the mutations. The selective footprint in fimH indicates that the pathoadaptive niche differentiation of E. coli is either in its initial stages or undergoing an evolutionary "source/sink" dynamic.
引用
收藏
页码:1373 / 1383
页数:11
相关论文
共 42 条
[1]   A KEY ROLE FOR TYPE-1 PILI IN ENTEROBACTERIAL COMMUNICABILITY [J].
BLOCH, CA ;
STOCKER, BAD ;
ORNDORFF, PE .
MOLECULAR MICROBIOLOGY, 1992, 6 (06) :697-701
[2]   NON-FLAGELLAR APPENDAGES OF BACTERIA [J].
BRINTON, CC .
NATURE, 1959, 183 (4664) :782-786
[3]   Evolutionary implications of the frequent horizontal transfer of mismatch repair genes [J].
Denamur, E ;
Lecointre, G ;
Darlu, P ;
Tenaillon, O ;
Acquaviva, C ;
Sayada, C ;
Sunjevaric, I ;
Rothstein, R ;
Elion, J ;
Taddei, F ;
Radman, M ;
Matic, I .
CELL, 2000, 103 (05) :711-721
[4]   The implications of a low rate of horizontal transfer in Borrelia [J].
Dykhuizen, DE ;
Baranton, G .
TRENDS IN MICROBIOLOGY, 2001, 9 (07) :344-350
[5]   How clonal is Staphylococcus aureus? [J].
Feil, EJ ;
Cooper, JE ;
Grundmann, H ;
Robinson, DA ;
Enright, MC ;
Berendt, T ;
Peacock, SJ ;
Smith, JM ;
Murphy, M ;
Spratt, BG ;
Moore, CE ;
Day, NPJ .
JOURNAL OF BACTERIOLOGY, 2003, 185 (11) :3307-3316
[6]   Recombination and the population structures of bacterial pathogens [J].
Feil, EJ ;
Spratt, BG .
ANNUAL REVIEW OF MICROBIOLOGY, 2001, 55 :561-590
[7]   Recombination within natural populations of pathogenic bacteria: Short-term empirical estimates and long-term phylogenetic consequences [J].
Feil, EJ ;
Holmes, EC ;
Bessen, DE ;
Chan, MS ;
Day, NPJ ;
Enright, MC ;
Goldstein, R ;
Hood, DW ;
Kalla, A ;
Moore, CE ;
Zhou, JJ ;
Spratt, BG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (01) :182-187
[8]  
FU YX, 1993, GENETICS, V133, P693
[9]   CLONAL DIVERGENCE IN ESCHERICHIA-COLI AS A RESULT OF RECOMBINATION, NOT MUTATION [J].
GUTTMAN, DS ;
DYKHUIZEN, DE .
SCIENCE, 1994, 266 (5189) :1380-1383
[10]   The FimH A27V mutation is pathoadaptive for urovirulence in Escherichia coli B2 phylogenetic group isolates [J].
Hommais, F ;
Gouriou, S ;
Amorin, C ;
Bui, H ;
Rahimy, MC ;
Picard, B ;
Denamur, E .
INFECTION AND IMMUNITY, 2003, 71 (06) :3619-3622