Variation in primary sequence and tandem repeat copy number among i-antigens of Ichthyophthirius multifiliis[Mol. Biochem. Parasitol. 120 (2002) 93–106]

2002 ◽  
Vol 122 (1) ◽  
pp. 117
Author(s):  
Yuankai Lin ◽  
Tian Long Lin ◽  
Chia-Ching Wang ◽  
Xuting Wang ◽  
Knut Stieger ◽  
...  
2002 ◽  
Vol 120 (1) ◽  
pp. 93-106 ◽  
Author(s):  
Yuankai Lin ◽  
Tian Long Lin ◽  
Chia-Cheng Wang ◽  
Xuting Wang ◽  
Knut Stieger ◽  
...  

BMC Genomics ◽  
2010 ◽  
Vol 11 (1) ◽  
Author(s):  
Deanna C Tremblay ◽  
Graham Alexander ◽  
Shawn Moseley ◽  
Brian P Chadwick

2006 ◽  
Vol 188 (12) ◽  
pp. 4253-4263 ◽  
Author(s):  
Amy J. Vogler ◽  
Christine Keys ◽  
Yoshimi Nemoto ◽  
Rebecca E. Colman ◽  
Zack Jay ◽  
...  

ABSTRACT Variable-number tandem repeat (VNTR) loci have shown a remarkable ability to discriminate among isolates of the recently emerged clonal pathogen Escherichia coli O157:H7, making them a very useful molecular epidemiological tool. However, little is known about the rates at which these sequences mutate, the factors that affect mutation rates, or the mechanisms by which mutations occur at these loci. Here, we measure mutation rates for 28 VNTR loci and investigate the effects of repeat copy number and mismatch repair on mutation rate using in vitro-generated populations for 10 E. coli O157:H7 strains. We find single-locus rates as high as 7.0 × 10−4 mutations/generation and a combined 28-locus rate of 6.4 × 10−4 mutations/generation. We observed single- and multirepeat mutations that were consistent with a slipped-strand mispairing mutation model, as well as a smaller number of large repeat copy number mutations that were consistent with recombination-mediated events. Repeat copy number within an array was strongly correlated with mutation rate both at the most mutable locus, O157-10 (r 2 = 0.565, P = 0.0196), and across all mutating loci. The combined locus model was significant whether locus O157-10 was included (r 2 = 0.833, P < 0.0001) or excluded (r 2 = 0.452, P < 0.0001) from the analysis. Deficient mismatch repair did not affect mutation rate at any of the 28 VNTRs with repeat unit sizes of >5 bp, although a poly(G) homomeric tract was destabilized in the mutS strain. Finally, we describe a general model for VNTR mutations that encompasses insertions and deletions, single- and multiple-repeat mutations, and their relative frequencies based upon our empirical mutation rate data.


2019 ◽  
Author(s):  
Colin J. Raposo ◽  
Kyle A. McElroy ◽  
Stephen M. Fuchs

AbstractThe pathogenic yeast Candida glabrata is reliant on a suite of cell surface adhesins that play a variety of roles necessary for transmission, establishment, and proliferation during infection. One particular adhesin, Epithelial Adhesin 1 [Epa1p], is responsible for binding to host tissue, a process which is essential for fungal propagation. Epa1p structure consists of three domains: an N-terminal intercellular binding domain responsible for epithelial cell binding, a C-terminal GPI anchor for cell wall linkage, and a serine / threonine-rich linker domain connecting these terminal domains. The linker domain contains a 40-amino acid tandem repeat region, which we have found to be variable in repeat copy number between isolates from clinical sources. We hypothesized that natural variation in Epa1p repeat copy may modulate protein function. To test this, we recombinantly expressed Epa1p with various repeat copy numbers in S. cerevisiae to determine how differences in repeat copy number affect Epa1p expression, surface display, and binding to human epithelial cells. Our data suggest that repeat copy number variation has pleiotropic effects, influencing gene expression, protein surface display, shedding from the cell surface, and host tissue adhesion of the Epa1p adhesin. Understanding these links between repeat copy number variants and mechanisms of infection provide new understanding of the variety of roles of repetitive proteins contribute to pathogenicity of C. glabrata.


2009 ◽  
Vol 282 (4) ◽  
pp. 395-406 ◽  
Author(s):  
R. Navajas-Pérez ◽  
M. E. Quesada del Bosque ◽  
M. A. Garrido-Ramos

1998 ◽  
Vol 10 (11) ◽  
pp. 1915
Author(s):  
Mark S. Dixon ◽  
Kostas Hatzixanthis ◽  
David A. Jones ◽  
Kate Harrison ◽  
Jonathan D. G. Jones

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