Disease relevance of dinD

• The most consistently activated E. coli promoters were those for genes micF, osmY, and dinD [1].
• Several notable examples include the discovery of a LexA-like protein, HdiR, in Lactococcus lactis, organisms with two lexA genes, and small DNA damage-inducible cassettes under LexA control [2].
• Myxococcus xanthus, a member of the Proteobacteria delta-class, has two independent recA genes, recA1 and recA2, but only recA2 is DNA damage-inducible [3].
• DNA damage-inducible (din) genes in Bacillus subtilis are coordinately regulated and together compose a global regulatory network that has been termed the SOS-like or SOB regulon [4].
• Identification of some DNA damage-inducible genes of Mycobacterium tuberculosis: apparent lack of correlation with LexA binding [5].

High impact information on dinD

• Human myxoid liposarcomas contain a characteristic chromosomal translocation, t(12;16)(q13;p11), that is associated with a structural rearrangement of the gene encoding CHOP, a growth arrest and DNA-damage inducible member of the C/EBP family of transcription factors residing on 12q13 [6].
• Homologous recombination-dependent initiation of DNA replication from DNA damage-inducible origins in Escherichia coli [7].
• DNA polymerase II is encoded by the DNA damage-inducible dinA gene of Escherichia coli [8].
• The cluster of genes that encode for the three characterized protein components of sMMO (MMOH, MMOB, and MMOR) contains an additional open reading frame (orfY) of unknown function [9].
• The Escherichia coli UVM (UV Modulation of mutagenesis) response is a DNA damage-inducible mutagenic pathway detected as significantly increased mutagenesis at 3,N4-ethenocytosine (epsilon C) lesions borne on transfected single-stranded M13 vector DNA [10].

Biological context of dinD

• Identification of high affinity binding sites for LexA which define new DNA damage-inducible genes in Escherichia coli [11].
• The orfE, orfX, and orfY genes were inactivated on the bacterial chromosome by deletion-insertion mutagenesis using a kanamycin resistance cassette [12].
• Inactivation of these genes (designated orfE, orfX and orfY) by crossing the KmR-cassette-disrupted orf into the chromosome indicated that they were not required during exponential growth (Poulsen et al., Mol., Microbiol., 1989 b) [13].
• These observations suggest that the increased protection afforded to P. aeruginosa by R2 is derived from a RecA-mediated, DNA-damage-inducible, error-prone DNA repair system which complements the lack of a chromosomally encoded umuDC-like operon [14].
• In this study, we have analyzed the expression following DNA damage in M. tuberculosis of a number of other genes which are DNA damage inducible in Escherichia coli [5].

Associations of dinD with chemical compounds

• In addition, dinB and dinD in the presence of both nalidixic acid and H2O2 at the same time showed no synergistic responses [15].

Other interactions of dinD

• A palindromic sequence, 5'-GAACNGTTC-3', which is identical to the consensus sequence found within the putative promoter region of the Bacillus subtilis DNA damage-inducible genes, was located within the promoter region of uvrA [16].
• These observations lead us to deduce that S. typhimurium has at least one DNA damage-inducible locus in addition to recA that is required for UV mutability [17].
• The uvrB gene of Pseudomonas aeruginosa is not DNA damage inducible [18].
• The hyperthermophilic archaeon, Pyrococcus (strain IFREMER AL585), contains an ORF that encodes a polypeptide with a high similarity to the Escherichia coli dinF (DNA damage-inducible) gene product [19].
• Analysis of transcriptional fusions with the lacZ gene demonstrates that, contrary to what happens with its homologous gene of E. coli, the P. aeruginosa uvrA gene is not DNA damage-inducible [20].

Analytical, diagnostic and therapeutic context of dinD

• Insertion of the element was site specific, as PCR and Southern blotting analysis revealed that the erm(B) element was inserted into orfY, a gene of unknown function [21].

References