Editing Staphylococcus aureus (section)

=== Strategies for post-transcriptional regulation by 3'untranslated region ===
Many [[Messenger RNA|mRNAs]] in ''S. aureus'' carry [[three prime untranslated region]]s (3'UTR) longer than 100 [[nucleotide]]s, which may potentially have a regulatory function.<ref name="Mozos">{{cite journal | vauthors = Ruiz de los Mozos I, Vergara-Irigaray M, Segura V, Villanueva M, Bitarte N, Saramago M, Domingues S, Arraiano CM, Fechter P, Romby P, Valle J, Solano C, Lasa I, Toledo-Arana A | title = Base pairing interaction between 5'- and 3'-UTRs controls icaR mRNA translation in ''Staphylococcus aureus'' | journal = PLOS Genetics | volume = 9 | issue = 12 | pages = e1004001 | date = 2013 | pmid = 24367275 | pmc = 3868564 | doi = 10.1371/journal.pgen.1004001 | doi-access = free }}</ref>

Further investigation of i''caR'' mRNA (mRNA coding for the repressor of the main expolysaccharidic compound of the bacteria biofilm matrix) demonstrated that the 3'UTR binding to the [[Five prime untranslated region|5' UTR]] can interfere with the translation initiation complex and generate a double stranded substrate for [[Ribonuclease III|RNase III]]. The interaction is between the UCCCCUG motif in the 3'UTR and the [[Shine-Dalgarno sequence|Shine-Dalagarno]] region at the 5'UTR. Deletion of the motif resulted in IcaR repressor accumulation and inhibition of biofilm development.<ref name= Mozos/> The biofilm formation is the main cause of ''Staphylococcus'' implant infections.<ref>{{cite journal | vauthors = Arciola CR, Campoccia D, Speziale P, Montanaro L, Costerton JW | title = Biofilm formation in Staphylococcus implant infections. A review of molecular mechanisms and implications for biofilm-resistant materials | journal = Biomaterials | volume = 33 | issue = 26 | pages = 5967–82 | date = September 2012 | pmid = 22695065 | doi = 10.1016/j.biomaterials.2012.05.031 }}</ref>