Activating Compound | Comment | Organism | Structure |
---|---|---|---|
nitrite | acidic nitrite enhanced the bactericidal effect of stabilized topoisomerase I cleavage complex | Escherichia coli |
Application | Comment | Organism |
---|---|---|
medicine | bacterial topoisomerase I is a therapeutic target | Escherichia coli |
Cloned (Comment) | Organism |
---|---|
gene topA, the gene is controlled by four promoters recognized by sigma32 and sigmas in addition to sigma70 | Escherichia coli |
Protein Variants | Comment | Organism |
---|---|---|
D117N | site-directed mutagenesis, induction of mutant YpTOP1-D117N topoisomerase by arabinose is similar in the absence or presence of trimethoprim | Escherichia coli |
additional information | usage of isogenic topA+ strain RFM44526 to study the involvement of topoisomerase I function in the SOS response. To monitor the extent of cell killing from accumulation of the topoisomerase I cleavage complex, Escherichia coli strain BW117N with a mutant Yersinia pestis topoisomerase I, YpTOP1-D117N, gene under the control of the BAD promoter inserted into the chromosome36 is used | Escherichia coli |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Escherichia coli | - |
gene topA | - |
Escherichia coli RFM475 | - |
gene topA | - |
Synonyms | Comment | Organism |
---|---|---|
Topoisomerase I | - |
Escherichia coli |
Organism | Comment | Expression |
---|---|---|
Escherichia coli | trimethoprim, mitomycin C, or acidified nitrite induce the enzyme | up |
General Information | Comment | Organism |
---|---|---|
additional information | induction of mutant YpTOP1-D117N topoisomerase I in Escherichia coli strain BW117N with 0.002%-0.02% arabinose results in a 104-105fold decrease in viability due to the lethal stabilized covalent complex | Escherichia coli |
physiological function | bacterial topoisomerase I plays a major role in preventing excessive negative supercoiling of DNA and its function is actively involved in the SOS response to antibiotics and stress challenge. Cell killing initiated by the topoisomerase I cleavage complex is enhanced by antibiotics and the host response. During rapid transcription at gene loci induced by the stress response, movement of the RNA polymerase complex leads to increased negative supercoiling behind the complex. Topoisomerase I is needed to prevent hypernegative supercoiling and R-loop formation, which would otherwise inhibit the expression of the stress response genes. Topoisomerase I function is required for efficient transcriptional activation of the recA and dinD1 promoters during the Escherichia coli SOS response to trimethoprim and mitomycin C | Escherichia coli |