Journal
NUCLEIC ACIDS RESEARCH
Volume 32, Issue 2, Pages 848-854Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkh219
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R37AI030492, R01AI030492, T32AI007210, R29AI030492] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK052574] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM019422, R37GM019422] Funding Source: NIH RePORTER
- NIAID NIH HHS [T32 AI07210-17, AI030492, R37 AI030492, R01 AI030492, T32 AI007210] Funding Source: Medline
- NIDDK NIH HHS [P30 DK052574, P30 DK52574] Funding Source: Medline
- NIGMS NIH HHS [R37 GM019422, R01 GM019422, GM19422] Funding Source: Medline
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The type III secretion system involved in Salmonella enterica serovar Typhimurium invasion of host cells has been disrupted using inducibly expressed oligonucleotide external guide sequences (EGSs) complementary to invB or invC mRNA. These EGSs direct single site cleavage in these mRNAs by endogenous RNase P, and their expression in Salmonella results in invC mRNA and InvC protein depletion, decreased type III secretion and interference with host cell invasion. Comparison of these effects with those from studies of Salmonella invB and invC mutants suggests that invB EGSs have polar effects on invC mRNA.
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