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. 2008 Jun 13;190(16):5690–5698. doi: 10.1128/JB.00314-08

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FIG. 8. — Model of GelE-mediated lysis in E. faecalis biofilm development. The model presents two mechanisms by which GelE could mediate lytic activity. The first mechanism is referred to as autolysis (A), and gelatinase () from the producer cell could activate a putative autolysin (▴) on the cell surface, resulting in autolysis. The presence of SprE () is predicted to regulate the GelE-mediated autolysin activation. The second mechanism, referred to as fratricide (allolysis) (B), allows for the diffusion of GelE () from the producer cell (A) to a susceptible sibling (B), wherein the sibling cell undergoes lysis following autolysin (▴) activation by GelE. The extent of bystander or sibling lysis would potentially be regulated by the presence of SprE () in the environment. The mechanism of SprE-mediated regulation is unknown but may involve alteration of the putative autolysin, rendering it to an inactive form (▪).

Inline graphic — Model of GelE-mediated lysis in E. faecalis biofilm development. The model presents two mechanisms by which GelE could mediate lytic activity. The first mechanism is referred to as autolysis (A), and gelatinase () from the producer cell could activate a putative autolysin (▴) on the cell surface, resulting in autolysis. The presence of SprE () is predicted to regulate the GelE-mediated autolysin activation. The second mechanism, referred to as fratricide (allolysis) (B), allows for the diffusion of GelE () from the producer cell (A) to a susceptible sibling (B), wherein the sibling cell undergoes lysis following autolysin (▴) activation by GelE. The extent of bystander or sibling lysis would potentially be regulated by the presence of SprE () in the environment. The mechanism of SprE-mediated regulation is unknown but may involve alteration of the putative autolysin, rendering it to an inactive form (▪).