The Genetic Architecture Of The S. Aureus Leucocidins: Case Study

II-Leukocidin genetic organization and genome distribution

The genetic architecture of the S. aureus leucocidins is widely conserved. F and S subunits of a certain toxin pair are transcribed from specific single promoter. The open reading frame of the S subunit immediately come before The open reading frameof the F subunit, with as little as a single nucleotide separating each open reading frames (Fig.1). The only known exception to this rule iwas in gamma-hemolysin locus.

1-Gamma-hemolysin:

Gamma-hemolysin has a genetic locus which consist of three open reading frames that sits within the core genome of S. aureus (Fig. 1) .The HlgC and HlgA genes encode the HlgCB toxin while HlgA with HlgB encode HlgAB toxin. The transcribed HlgA gene
1). Hlb encodes beta-hemolysin that has hemolytic acivity on blood agar (Dinges et al., 2000). More studies are needed to find out if LukAB/HG gene is uniformly conserved in all S. aureus isolates.

3- LUKED:

In contrast to gamma-hemolysin and LukAB/HG, lukED genes are outside core genome. They present in S. aureus pathogenicity island (SaPI) vSaβ which is an immobile genatice element . Some genes such as enterotoxins genes and serine proteases are encoded inside the pathogenicity island (SaPI) (Baba et al., 2008; Gill, 2009).

LukED genes are absent in some lineage including clonal complexes (CCs) 22, 42, 75 and 431, beacuse of luk ED is lineage specific. Also, LukED exhibits little sequence variance through sequenced S. aureus strains (McCarthy and Lindsay, 2013).
(Table. 1), characteristics of the leukocidins of S. aureus. 4- PVL and
A subunit-dependent binding to cellular membranes was also observed (Woodin and Wieneke, 1966; Woodin and Wieneke, 1967). Follow-up studies by Noda et al. confirmed increasing in calcium influx upon treatment with leucocidin (HlgCB) and binding of the toxin to host cell membranes (Noda et al., 1982). However, none of above studies definitively recognized pore formation as a mechanism of leukocidin action.
Finck Barbancon and colleagues performed certain studies to measure calcium and ethidium bromide entry into PMNs upon treatment with purified PVL toxin, It was supposed that ethidium entry into host cells, but not calcium entry, is a definitive marker of pore formation by leucocidins (Finck-Barbancon et al., 1992). It was found that calcium entry upon treatment with purifed lukSF is believed to occur after pore formation and is mediated by the divalent cation channels (Baba Moussa et al.,