The UvrA-like protein Ecm16 requires ATPase activity to render resistance against echinomycin.
The UvrA-like protein Ecm16 requires ATPase activity to render resistance against echinomycin.
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UvrA样蛋白Ecm16需要ATPase活性才能对棘球菌素产生抗性。
DOI：
10.1111/mmi.14918
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发表时间：
2022-06
影响因子：
3.6
通讯作者：
Mera, Paola E.
中科院分区：
文献类型：
--
作者：
Erlandson, Amanda;Gade, Priyanka;Menikpurage, Inoka P.;Kim, Chu-Young;Mera, Paola E.
Bacteria use various strategies to become antibiotic resistant. The molecular details of these strategies are not fully understood. We can increase our understanding by investigating the same strategies found in antibiotic‐producing bacteria. In this work, we characterize the self‐resistance protein Ecm16 encoded by echinomycin‐producing bacteria. Ecm16 is a structural homolog of the nucleotide excision repair protein UvrA. Expression of ecm16 in the heterologous system Escherichia coli was sufficient to render resistance against echinomycin. Ecm16 binds DNA (double‐stranded and single‐stranded) using a nucleotide‐independent binding mode. Ecm16’s binding affinity for DNA increased by 1.7‐fold when the DNA is intercalated with echinomycin. Ecm16 can render resistance against echinomycin toxicity independently of the nucleotide excision repair system. Similar to UvrA, Ecm16 has ATPase activity, and this activity is essential for Ecm16’s ability to render echinomycin resistance. Notably, UvrA and Ecm16 were unable to complement each other's function. Together, our findings identify new mechanistic details of how a refurbished DNA repair protein Ecm16 can specifically render resistance to the DNA intercalator echinomycin. How do drug‐producer bacteria protect themselves from the toxicity of those drugs? We show that bacteria can make proteins such as Ecm16 is quite similar to a conserved DNA‐intercalator echinomycin. Ecm16 looks like a conserved DNA‐repair protein and requires ATP, yet its mechanism of action is different.
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影响因子：
4.8
作者：
Gunz, D;Hess, MT;Naegeli, H
通讯作者：
Naegeli, H
影响因子：
15
作者：
DELL, A;WILLIAMS, DH;ROBERTS, GCK
通讯作者：
ROBERTS, GCK
DOI：
10.1073/pnas.51.2.293
发表时间：
1964-01-01
影响因子：
11.1
作者：
BOYCE, RP;HOWARDFLANDERS, P
通讯作者：
HOWARDFLANDERS, P
DOI：
10.1073/pnas.82.15.4925
发表时间：
1985-01-01
影响因子：
11.1
作者：
CARON, PR;KUSHNER, SR;GROSSMAN, L
通讯作者：
GROSSMAN, L
DOI：
10.1016/b978-0-12-387665-2.00001-8
发表时间：
2012
影响因子：
--
作者：
Kad, Neil M.;Van Houten, Bennett
通讯作者：
Van Houten, Bennett