Prepiak Peter, Dubnau David
Public Health Research Institute, 225 Warren Street, Newark, NJ 07103, USA.
Mol Cell. 2007 Jun 8;26(5):639-47. doi: 10.1016/j.molcel.2007.05.011.
ComS is an antiadaptor protein that binds to MecA, displacing the competence transcription factor ComK. This protects ComK from degradation by the ClpCP protease and turns on the switch leading to bistable gene expression. Here we identify the motifs on ComK and ComS that mediate binding to MecA, and we show that they contain similar core sequences (FMLYPK and IILYPR, respectively), located near the C and N termini of the respective proteins. A 17 residue peptide from ComK including this sequence has the same affinity for MecA as full-length ComK, and a peptide containing this sequence is sufficient to target green fluorescent protein for degradation in vivo. Crosslinking and competition experiments demonstrate that ComK- and ComS-derived peptides bind to the same region of MecA. We propose a model in which the antiadaptor protein ComS acts by direct competition to protect ComK from degradation.
ComS是一种抗适配蛋白，它与MecA结合，取代感受态转录因子ComK。这保护ComK不被ClpCP蛋白酶降解，并开启导致双稳态基因表达的开关。在这里，我们确定了ComK和ComS上介导与MecA结合的基序，并且我们表明它们包含相似的核心序列（分别为FMLYPK和IILYPR），位于各自蛋白质的C端和N端附近。来自ComK的包含该序列的17个残基肽对MecA的亲和力与全长ComK相同，并且包含该序列的肽足以在体内靶向绿色荧光蛋白进行降解。交联和竞争实验表明，来自ComK和ComS的肽与MecA的同一区域结合。我们提出了一个模型，其中抗适配蛋白ComS通过直接竞争来保护ComK不被降解。
