MecA
Revision as of 09:55, 14 May 2013 by 134.76.70.252 (talk)
- Description: buffering protein for development, dampens transitions to spore, biofilm exopolysaccharide and competence expression , targets ComK to ClpC-ClpP degradation machine (in log Phase), inhibits the transcriptional activity of Spo0A∼P by direct interaction
Gene name | mecA |
Synonyms | |
Essential | no |
Product | adaptor protein |
Function | control of ComK degradation, regulation of competence |
Gene expression levels in SubtiExpress: mecA | |
Interactions involving this protein in SubtInteract: MecA | |
MW, pI | 25 kDa, 4.209 |
Gene length, protein length | 654 bp, 218 aa |
Immediate neighbours | yjbE, coiA |
Sequences | Protein DNA DNA_with_flanks |
Genetic context This image was kindly provided by SubtiList
| |
Expression at a glance PubMed |
Contents
Categories containing this gene/protein
genetic competence, proteolysis
This gene is a member of the following regulons
The gene
Basic information
- Locus tag: BSU11520
Phenotypes of a mutant
Database entries
- DBTBS entry: [1]
- SubtiList entry: [2]
Additional information
The protein
Basic information/ Evolution
- Catalyzed reaction/ biological activity:
- Protein family: mecA family (according to Swiss-Prot)
- Paralogous protein(s): YpbH
Extended information on the protein
- Kinetic information:
- Domains:
- Modification:
- Cofactor(s):
- Effectors of protein activity:
Database entries
- UniProt: P37958
- KEGG entry: [3]
- E.C. number:
Additional information
Expression and regulation
- Regulation:
- Regulatory mechanism:
- Additional information:
Biological materials
- Mutant: GP813 (spc), GP814 (aphA3) both available in the Stülke lab
- Expression vector:
- lacZ fusion:
- GFP fusion:
- two-hybrid system:
- Antibody:
Labs working on this gene/protein
Your additional remarks
References
Reviews
Additional reviews: PubMed
Aurelia Battesti, Susan Gottesman
Roles of adaptor proteins in regulation of bacterial proteolysis.
Curr Opin Microbiol: 2013, 16(2);140-7
[PubMed:23375660]
[WorldCat.org]
[DOI]
(I p)
Original Publications
Additonal publications: PubMed