TY - JOUR
T1 - Abrogation of the Twin Arginine Transport system in Salmonella enterica serovar Typhimurium leads to colonization defects during infection
AU - Reynolds, M. Megan
AU - Bogomolnaya, Lydia
AU - Guo, Jinbai
AU - Aldrich, Lindsay
AU - Bokhari, Danial
AU - Santiviago, Carlos A.
AU - McClelland, Michael
AU - Andrews-Polymenis, Helene
PY - 2011
Y1 - 2011
N2 - TatC (STM3975) is a highly conserved component of the Twin Arginine Transport (Tat) systems that is required for transport of folded proteins across the inner membrane in gram-negative bacteria. We previously identified a ΔtatC mutant as defective in competitive infections with wild type ATCC14028 during systemic infection of Salmonella-susceptible BALB/c mice. Here we confirm these results and show that the ΔtatC mutant is internalized poorly by cultured J774-A.1 mouse macrophages a phenotype that may be related to the systemic infection defect. This mutant is also defective for short-term intestinal and systemic colonization after oral infection of BALB/c mice and is shed in reduced numbers in feces from orally infected Salmonella-resistant (CBA/J) mice. We show that the ΔtatC mutant is highly sensitive to bile acids perhaps resulting in the defect in intestinal infection that we observe. Finally, the ΔtatC mutant has an unusual combination of motility phenotypes in Salmonella; it is severely defective for swimming motility but is able to swarm well. The ΔtatC mutant has a lower amount of flagellin on the bacterial surface during swimming motility but normal levels under swarming conditions.
AB - TatC (STM3975) is a highly conserved component of the Twin Arginine Transport (Tat) systems that is required for transport of folded proteins across the inner membrane in gram-negative bacteria. We previously identified a ΔtatC mutant as defective in competitive infections with wild type ATCC14028 during systemic infection of Salmonella-susceptible BALB/c mice. Here we confirm these results and show that the ΔtatC mutant is internalized poorly by cultured J774-A.1 mouse macrophages a phenotype that may be related to the systemic infection defect. This mutant is also defective for short-term intestinal and systemic colonization after oral infection of BALB/c mice and is shed in reduced numbers in feces from orally infected Salmonella-resistant (CBA/J) mice. We show that the ΔtatC mutant is highly sensitive to bile acids perhaps resulting in the defect in intestinal infection that we observe. Finally, the ΔtatC mutant has an unusual combination of motility phenotypes in Salmonella; it is severely defective for swimming motility but is able to swarm well. The ΔtatC mutant has a lower amount of flagellin on the bacterial surface during swimming motility but normal levels under swarming conditions.
UR - http://www.scopus.com/inward/record.url?scp=79551549660&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79551549660&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0015800
DO - 10.1371/journal.pone.0015800
M3 - Article
C2 - 21298091
AN - SCOPUS:79551549660
SN - 1932-6203
VL - 6
JO - PloS one
JF - PloS one
IS - 1
M1 - e15800
ER -