|ralR||Rac prophage; Toxic component of a type I toxin-antitoxin (TA) system. Upon overexpression inhibits growth and reduces colony-forming units in both the presence and absence of the Rac prophage, cells become filamentous. Has deoxyribonuclease activity (probably endonucleolytic), does not digest RNA. Its toxic effects are neutralized by sRNA antitoxin RalA, which is encoded in trans on the opposite DNA strand. Has RAL-like activity. (64 aa)|| |
Predicted Functional Partners:
DUF1187 family protein, Rac prophage; Helps to maintain the integrity of the chromosome by lowering the steady-state level of double strand breaks. This region of DNA acts as an antitoxin to toxin RalR, a DNase, but it seems to be sRNA RalA that has the antitoxin activity and not this putative protein. Therefore the identity of this as a protein-coding gene has been cast into doubt.
| || || || || ||0.969
Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ.
| || || || || ||0.949
Rac prophage; Putative lambdoid prophage Rac excisionase.
| || || || || ||0.917
Toxic peptide regulated by antisense sRNA symR; Toxic component of a type I toxin-antitoxin (TA) system. Involved in the degradation and recycling of damaged RNA. It is itself a target for degradation by the ATP-dependent protease Lon. Belongs to the SymE family.
| || || || || || ||0.810
UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family.
| || || || || || || ||0.809
Toxic membrane persister formation peptide, LexA-regulated; Toxic component of a type I toxin-antitoxin (TA) system (Probable). Overexpression causes cessation of growth, induces stress-response, a number of membrane protein genes, and leads to cell death. Inhibits ATP synthesis, ATP levels drop drastically quickly after induction. Part of the programmed response to DNA damage; damage leads to increased accumulation of the protein which slows or stops bacterial growth, probably allowing DNA repair before cells continue to grow.
| || || || || || || ||0.801
| || || || || ||0.798
Rac prophage; Binds to single-stranded DNA and also promotes the renaturation of complementary single-stranded DNA. Function in recombination. Has a function similar to that of lambda RedB.
| || || || || ||0.789
Toxic membrane protein; Toxic component of a type I toxin-antitoxin (TA) system. May be a toxic protein; overexpression causes cessation of growth and rapid membrane depolarization. Overexpression induces stress-response and a number of membrane protein genes.
| || || || || || || ||0.789
Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...]
| || || || || || || ||0.785