SprD
| SprD | |
|---|---|
 Conserved secondary structure of SprD. | |
| Identifiers | |
| Symbol | SprD |
| Rfam | RF01828 |
| Other data | |
| RNA type | Gene |
| Domain(s) | Staphylococcus aureus |
| PDB structures | PDBe |
In molecular biology SprD (Small pathogenicity island RNA D) is a non-coding RNA expressed on pathogenicity islands in Staphylococcus aureus.[1] It was identified in silico along with a number of other sRNAs (SprA-G) through microarray analysis which were confirmed using a Northern blot.[2] SprD has been found to significantly contribute to causing disease in an animal model.[1]
Function
[edit]SprD is located between genes scn and chp in the innate immune evasion cluster (IEC) of the S. aureus genome. Its placement within this region was the first indication of a virulence-factor regulatory function.[1]
SprD binds with sbi (Staphylococcus aureus binder of IgG)[3] mRNA which encodes an immune evasion protein. It occludes the Shine-Dalgarno sequence and the initiation codon of sbi, forming a sbi mRNA-SprD duplex repressing the translation of the mRNA.[1]
sbi protein interferes with the host's innate immune response by binding Factor H, Complement component 3 and IgG.[3][4]
See also
[edit]References
[edit]- ^ a b c d Chabelskaya S, Gaillot O, Felden B (June 2010). "A Staphylococcus aureus small RNA is required for bacterial virulence and regulates the expression of an immune-evasion molecule". PLOS Pathog. 6 (6): e1000927. doi:10.1371/journal.ppat.1000927. PMC 2880579. PMID 20532214.
{{cite journal}}: CS1 maint: article number as page number (link) - ^ Pichon C, Felden B (October 2005). "Small RNA genes expressed from Staphylococcus aureus genomic and pathogenicity islands with specific expression among pathogenic strains". Proc. Natl. Acad. Sci. U.S.A. 102 (40): 14249–14254. doi:10.1073/pnas.0503838102. PMC 1242290. PMID 16183745.
- ^ a b Haupt K, Reuter M, van den Elsen J, et al. (December 2008). "The Staphylococcus aureus protein Sbi acts as a complement inhibitor and forms a tripartite complex with host complement Factor H and C3b". PLOS Pathog. 4 (12): e1000250. doi:10.1371/journal.ppat.1000250. PMC 2602735. PMID 19112495.
{{cite journal}}: CS1 maint: article number as page number (link) - ^ Zhang L, Jacobsson K, Vasi J, Lindberg M, Frykberg L (April 1998). "A second IgG-binding protein in Staphylococcus aureus". Microbiology. 144 (4): 985–991. doi:10.1099/00221287-144-4-985. PMID 9579072. Retrieved 2010-08-09.
Further reading
[edit]- Upadhyay A, Burman JD, Clark EA, et al. (August 2008). "Structure-function analysis of the C3 binding region of Staphylococcus aureus immune subversion protein Sbi". J. Biol. Chem. 283 (32): 22113–22120. doi:10.1074/jbc.M802636200. PMC 2494919. PMID 18550524.
- Burman JD, Leung E, Atkins KL, et al. (June 2008). "Interaction of human complement with Sbi, a staphylococcal immunoglobulin-binding protein: indications of a novel mechanism of complement evasion by Staphylococcus aureus". J. Biol. Chem. 283 (25): 17579–17593. doi:10.1074/jbc.M800265200. PMC 2649420. PMID 18434316.
- Atkins KL, Burman JD, Chamberlain ES, et al. (March 2008). "S. aureus IgG-binding proteins SpA and Sbi: host specificity and mechanisms of immune complex formation". Mol. Immunol. 45 (6): 1600–1611. doi:10.1016/j.molimm.2007.10.021. PMID 18061675.
- Chabelskaya S, Bordeau V, Felden B (Apr 1, 2014). "Dual RNA regulatory control of a Staphylococcus aureus virulence factor". Nucleic Acids Research. 42 (8): 4847–4858. doi:10.1093/nar/gku119. PMC 4005698. PMID 24510101.