TADB
TA Pair: PHD-Fic
#OrganismToxinAntitoxinLocus IDReplicon
1Cronobacter sakazakii ATCC BAA-8944478 ESA_04289ESA_04288NC_009778
2Desulfitobacterium hafniense Y512478 DSY3332DSY3334NC_007907
3Desulfotomaculum reducens MI-13658 Dred_3007Dred_3006NC_009253
4Dinoroseobacter shibae DFL 12 = DSM 164934732 Dshi_4113Dshi_4112NC_009958
5Escherichia coli 15206150 IPF_70aIPF_68NC_010558
6Klebsiella pneumoniae subsp. pneumoniae MGH 785784248 KPN_03814KPN_03815NC_009648
7Lactobacillus salivarius UCC1182548 LSL_1388LSL_1389NC_007929
8Marinomonas sp. MWYL14268 Mmwyl1_4024Mmwyl1_4023NC_009654
9Pectobacterium atrosepticum SCRI10431099 ECA0253ECA0254NC_004547
10Photorhabdus luminescens subsp. laumondii TTO11216 plu2255plu2254NC_005126
11Salmonella enterica arizonae serovar 62 z4 z23 RSK29804781 SARI_01417SARI_01418NC_010067
12Salmonella enterica subsp. enterica serovar Dublin str. CT 020218535980 SeD_A3929SeD_A3930NC_011205
13Salmonella enterica subsp. enterica serovar Paratyphi B str. SPB74805 SPAB_04420SPAB_04421NC_010102
14Salmonella enterica subsp. enterica serovar Typhimurium str. LT2442 STM3558STM3559NC_003197
15Yersinia enterocolitica subsp. enterocolitica 80813482 YE2032YE2033NC_008800


Antitoxin domain: PHD. PHD folds into an interleaved type of Zn-finger chelating 2 Zn ions in a similar manner to that of the RING and FYVE domains. Several PHD fingers have been identified as binding modules of methylated histone H3.

Toxin domain: Fic. Fic/Doc family. This family consists of the Fic (filamentation induced by cAMP) protein and doc (death on curing). The Fic protein is involved in cell division and is suggested to be involved in the synthesis of PAB or folate, indicating that the Fic protein and cAMP are involved in a regulatory mechanism of cell division via folate metabolism. This family contains a central conserved motif HPFXXGNG in most members. The exact molecular function of these proteins is uncertain. P1 lysogens of Escherichia coli carry the prophage as a stable low copy number plasmid. The frequency with which viable cells cured of prophage are produced is about 10(-5) per cell per generation. A significant part of this remarkable stability can be attributed to a plasmid-encoded mechanism that causes death of cells that have lost P1. In other words, the lysogenic cells appear to be addicted to the presence of the prophage. The plasmid withdrawal response depends on a gene named doc (death on curing) that is represented by this family. Doc induces a reversible growth arrest of E. coli cells by targetting the protein synthesis machinery. Doc hosts the C-terminal domain of its antitoxin partner Phd (prevents host death) through fold complementation, a domain that is intrinsically disordered in solution but that folds into an alpha-helix on binding to Doc.


Structure
N/A
(1) Makarova KS et al. (2009) Comprehensive comparative-genomic analysis of type 2 toxin-antitoxin systems and related mobile stress response systems in prokaryotes. Biol Direct 4:19. [PudMed:19493340] in_silico