Growth of Escherichia coli in Human Urine: Role of Salt Tolerance and Accumulation of Glycine Betaine

1992 ◽  
Vol 166 (6) ◽  
pp. 1311-1315 ◽  
Author(s):  
C. M. Kunin ◽  
T. H. Hua ◽  
L. Van Arsdale White ◽  
M. Villarejo
2013 ◽  
Vol 66 (5) ◽  
pp. 428-436 ◽  
Author(s):  
Sylwia Wdowiak-Wróbel ◽  
Agnieszka Leszcz ◽  
Wanda Małek

2006 ◽  
Vol 74 (11) ◽  
pp. 6287-6292 ◽  
Author(s):  
Jerod A. Skyberg ◽  
Timothy J. Johnson ◽  
James R. Johnson ◽  
Connie Clabots ◽  
Catherine M. Logue ◽  
...  

ABSTRACT We have found an avian pathogenic Escherichia coli (APEC) plasmid, pAPEC-O2-ColV, which contains many of the genes associated with APEC virulence and also shows similarity in content to a plasmid and pathogenicity island of human uropathogenic E. coli (UPEC). To test the possible role of this plasmid in virulence, it was transferred by conjugation along with a large R plasmid, pAPEC-O2-R, into a commensal avian E. coli strain. The transconjugant was compared to recipient strain NC, UPEC strain HE300, and donor strain APEC O2 using various assays, including lethality for chicken embryos, growth in human urine, and ability to cause urinary tract infection in mice. The transconjugant killed significantly more chicken embryos than did the recipient. In human urine, APEC O2 grew at a rate equivalent to that of UPEC strain HE300, and the transconjugant showed significantly increased growth compared to the recipient. The transconjugant also significantly outcompeted the recipient in colonization of the murine kidney. These findings suggest that APEC plasmids, such as pAPEC-O2-ColV, contribute to the pathogenesis of avian colibacillosis. Moreover, since avian E. coli and their plasmids may be transmitted to humans, evaluation of APEC plasmids as possible reservoirs of urovirulence genes for human UPEC may be warranted.


1988 ◽  
Vol 263 (19) ◽  
pp. 9187-9198 ◽  
Author(s):  
J R Appleman ◽  
E E Howell ◽  
J Kraut ◽  
M Kühl ◽  
R L Blakley

2021 ◽  
Author(s):  
Mei Zheng ◽  
Jingchen Lin ◽  
Xingbei Liu ◽  
Wei Chu ◽  
Jinpeng Li ◽  
...  

Abstract Polyploidy occurs prevalently and plays an important role during plant speciation and evolution. This phenomenon suggests polyploidy could develop novel features that enable them to adapt wider range of environmental conditions compared with diploid progenitors. Bread wheat (Triticum aestivum L., BBAADD) is a typical allohexaploid species and generally exhibits greater salt tolerance than its tetraploid wheat progenitor (BBAA). However, little is known about the underlying molecular basis and the regulatory pathway of this trait. Here, we show that the histone acetyltransferase TaHAG1 acts as a crucial regulator to strengthen salt tolerance of hexaploid wheat. Salinity-induced TaHAG1 expression was associated with tolerance variation in polyploidy wheat. Overexpression, silencing and CRISPR-mediated knockout of TaHAG1 validated the role of TaHAG1 in salinity tolerance of wheat. TaHAG1 contributed to salt tolerance by modulating ROS production and signal specificity. Moreover, TaHAG1 directly targeted a subset of genes that are responsible for hydrogen peroxide production, and enrichment of TaHAG1 triggered increased H3 acetylation and transcriptional upregulation of these loci under salt stress. In addition, we found the salinity-induced TaHAG1-mediated ROS production pathway is involved in salt tolerance difference of wheat accessions with varying ploidy. Our findings provide insight into the molecular mechanism of how an epigenetic regulatory factor facilitates adaptability of polyploidy wheat and highlights this epigenetic modulator as a strategy for salt tolerance breeding in bread wheat.


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