Difference between revisions of "LytE"
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Revision as of 12:52, 16 May 2013
- Description: cell wall hydrolase (major autolysin), D,L-endopeptidase-type autolysin
Gene name | lytE |
Synonyms | papQ, cwlF |
Essential | no |
Product | cell wall hydrolase (major autolysin),endopeptidase-type autolysin |
Function | major autolysin, cell separation, cell proliferation |
Gene expression levels in SubtiExpress: lytE | |
MW, pI | 37 kDa, 10.713 |
Gene length, protein length | 1029 bp, 343 aa |
Immediate neighbours | phoA, citR |
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
cell wall degradation/ turnover
This gene is a member of the following regulons
SigH regulon, SigI regulon, Spo0A regulon, WalR regulon
The gene
Basic information
- Locus tag: BSU09420
Phenotypes of a mutant
- a cwlO lytE mutant is not viable PubMed
- growth defect at high temperature PubMed
- inactivation of lytE strongly restores beta-lactam resistance in a sigM mutant by delaying cell lysis PubMed
Database entries
- DBTBS entry: [1]
- SubtiList entry: [2]
Additional information
The protein
Basic information/ Evolution
- Catalyzed reaction/ biological activity:
- Protein family: nlpC/p60 family (according to Swiss-Prot)
- Paralogous protein(s): the C-terminal D,L-endopeptidase domains of LytE, LytF, CwlS, and CwlO exhibit strong sequence similarity
Extended information on the protein
- Kinetic information:
- Domains:
- C-terminal D,L-endopeptidase domain PubMed
- Modification:
- Cofactor(s):
- Effectors of protein activity:
Database entries
- Structure:
- UniProt: P54421
- KEGG entry: [3]
- E.C. number:
Additional information
Expression and regulation
- Operon: lytE PubMed
- Regulation:
- Regulatory mechanism:
- Additional information:
Biological materials
- Mutant:
- Expression vector:
- lacZ fusion:
- GFP fusion:
- two-hybrid system:
- Antibody:
Labs working on this gene/protein
Your additional remarks
References
Reviews
Additional reviews: PubMed
Original publications
Additional publications: PubMed