SMART: Pfam domain RelB

RelB

PFAM accession number:	PF04221
Interpro abstract (IPR007337):	Plasmids may be maintained stably in bacterial populations through the action of addiction modules, in which a toxin and antidote are encoded in a cassette on the plasmid. In any daughter cell that lacks the plasmid, the toxin persists and is lethal after the antidote protein is depleted. Toxin/antitoxin pairs are also found on main chromosomes, and likely represent selfish DNA. Sequences in the seed for this alignment all were found adjacent to toxin genes. Several toxin/antitoxin pairs may occur in a single species. RelE and RelB form a toxin-antitoxin system; RelE represses translation, probably through binding ribosomes [ (PUBMED:11274135) (PUBMED:12123459) ]. RelB stably binds RelE, presumably deactivating it. DinJ is an antitoxin component of a toxin-antitoxin (TA) module. It's a labile antitoxin that counteracts the effect of the YafQ toxin. YafQ and DinJ together bind their own promoter, and by analogy to other TA modules probably repress its expression. Cell death governed by the mazEF and dinJ-yafQ TA modules seems to play a role in biofilm formation [ (PUBMED:17263853) (PUBMED:19210620) (PUBMED:19707553) ].

PFAM accession number:

PF04221

Interpro abstract (IPR007337):

Plasmids may be maintained stably in bacterial populations through the action of addiction modules, in which a toxin and antidote are encoded in a cassette on the plasmid. In any daughter cell that lacks the plasmid, the toxin persists and is lethal after the antidote protein is depleted. Toxin/antitoxin pairs are also found on main chromosomes, and likely represent selfish DNA. Sequences in the seed for this alignment all were found adjacent to toxin genes. Several toxin/antitoxin pairs may occur in a single species. RelE and RelB form a toxin-antitoxin system; RelE represses translation, probably through binding ribosomes [ (PUBMED:11274135) (PUBMED:12123459) ]. RelB stably binds RelE, presumably deactivating it.

DinJ is an antitoxin component of a toxin-antitoxin (TA) module. It's a labile antitoxin that counteracts the effect of the YafQ toxin. YafQ and DinJ together bind their own promoter, and by analogy to other TA modules probably repress its expression. Cell death governed by the mazEF and dinJ-yafQ TA modules seems to play a role in biofilm formation [ (PUBMED:17263853) (PUBMED:19210620) (PUBMED:19707553) ].

This is a PFAM domain. For full annotation and more information, please see the PFAM entry RelB