Petcherski AG et al. (2000) Curr Biol "Mastermind is a putative activator for Notch."

[

Curr Biol,

2000]

During signaling by the Notch receptor, Notch's intracellular domain is cleaved, moves to the nucleus and associates with a DNA-binding protein of the CSL class (CSL for CBF1, Suppressor of Hairless (Su(H)), LAG-1); as a result, target genes are transcriptionally activated (reviewed in [1,2]). In Caenorhabditis elegans, a glutamine-rich protein called LAG-3 forms a ternary complex with the Notch intracellular domain and LAG-1 and appears to serve as a transcriptional activator that is critical for signaling [3]. Although database searches failed to identify a LAG-3-related protein, we surmised that Notch signaling in other organisms might involve an analogous activity.

Gibert L et al. (2014) FEMS Microbiol Lett "The major autolysin of Staphylococcus lugdunensis, AtlL, is involved in cell separation, stress-induced autolysis and contributes to bacterial pathogenesis."

Legris S, Gibert L, Lesouhaitier O, Marlinghaus L, Pons JL, Szabados F, Didi J, Pestel-Caron M

[

FEMS Microbiol Lett,

2014]

Staphylococcus lugdunensis is a human skin commensal organism, but it is considered as a virulent Staphylococcus species. In a previous study, we described the first S.lugdunensis autolysin, AtlL. This enzyme displays two enzymatic domains and generates two peptidoglycan hydrolases, an N-acetylmuramoyl-l-alanine amidase and an N-acetylglucosaminidase. In this study, to further investigate the functions of this autolysin, a atlL mutant was constructed. The microscopic examination of the mutant showed cell aggregates and revealed a rough outer cell surface demonstrating, respectively, the roles of AtlL in cell separation and peptidoglycan turnover. This atlL mutant exhibited a lower susceptibility to Triton X-100-induced autolysis assays and appears to be more resistant to cell wall antibiotic-induced lysis and death compared with its parental strain. The atlL mutation affected the biofilm formation capacity of S.lugdunensis. Furthermore, the atlL mutant showed trends toward reduced virulence using the Caenorhabditis elegans model. Overall, AtlL appears as a major cell wall autolysin of S.lugdunensis implicated in cell separation, in stress-induced autolysis and in bacterial pathogenesis.