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The weight of structural evidence favors the idea that an ATP-dependent ligase could be the ancestral point out from which NAD+-dependent ligases advanced, by acquisition of the specialized structural area (Ia) that binds the NMN leaving team. All recognised NAD+-dependent ligases have domain Ia, and they cannot use ATP as a substrate for ligase adenylylation, presumably mainly because LigA enzymes lack “motif IV” of the OB domain, the component of ATP-dependent DNA ligases that is assumed to interact with the PPi leaving group of ATP (five, 19). This “either/or” scenario of DNA ligase substrate specificity has been roiled by quite a few seemingly conflicting stories concerning the nucleotide specificity of archaeal DNA ligases.
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An engineered move three arrest mutant of DNA ligase would, if widely Energetic, pepper the genome with unresected five′-adenylates at sites of DNA restore or joining of Okazaki fragments. This would be catastrophic if the extent of DNA five′-adenylylation exceeds the cell's capacity to remove the lesions (33). This type of scenario is analogous to “poisoning” of topoisomerase IB by camptothecin medicine or drug-mimetic enzyme mutations that selectively impede the DNA ligation stage of the topoisomerase pathway.
S3), nonetheless the topology in the LigA clamp is starkly distinctive from that in the clamps fashioned by ChVLig and HuLig1. The kissing contacts that close the LigA clamp are sui generis
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