The two paralogous copies of the YoeB–YefM toxin–antitoxin module in Staphylococcus aureus differ in DNA binding and recognition patterns

Abstract

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Structural Analysis of Ino2p/Ino4p Mutual Interactions and Their Binding Interface with Promoter DNA

“…Our previous study demonstrated that the establishment of protein–DNA interaction might be associated with the recognition of both core and flanking sequences in the promoter DNA fragments [ 21 , 22 ]. To assess whether flanking sequences are critical to Ino2p DBD /Ino4p DBD /DNA mutual interaction, nucleotides corresponding to the flanking promoter DNA sequence were mutated (see Figure 5 A).…”

“…Taken together, these results suggest that residues (Ino2p His12/Glu16/Arg20/Arg44 and Ino4p His12/Glu16/Arg20 ) are critical for the optimal DNA binding affinity of the Ino2p DBD -Ino4p DBD heterodimer complex. Our previous study demonstrated that the establishment of protein-DNA interaction might be associated with the recognition of both core and flanking sequences in the promoter DNA fragments [21,22]. To assess whether flanking sequences are critical to Ino2p DBD /Ino4p DBD /DNA mutual interaction, nucleotides corresponding to the flanking promoter DNA sequence were mutated (see Figure 5A).…”

“…To assess whether flanking sequences are critical to Ino2p DBD /Ino4p DBD /DNA mutual interaction, nucleotides corresponding to the flanking promoter DNA sequence were mutated (see Figure 5A). The corresponding biochemical (EMSA and ITC) experiments demonstrated that the mutated flanking promoter fragment Our previous study demonstrated that the establishment of protein-DNA interaction might be associated with the recognition of both core and flanking sequences in the promoter DNA fragments [21,22]. To assess whether flanking sequences are critical to Ino2p DBD /Ino4p DBD /DNA mutual interaction, nucleotides corresponding to the flanking promoter DNA sequence were mutated (see Figure 5A).…”

Structural insights into the PrpTA toxin–antitoxin system in Pseudoalteromonas rubra

“…Toxin–antitoxin modules were initially identified as a plasmid stability factor in the conjugative plasmids in the 1980s ( Ogura and Hiraga, 1983 ; Jaffe et al, 1985 ; Gerdes et al, 1986 ; Cooper and Heinemann, 2000 ; Van Melderen, 2010 ; Ni et al, 2021 ). Later, they turned out to be widely distributed on the chromosomes and mobile genetic elements (MGEs) in bacteria, archaea, and bacteriophage, especially pathogenic bacteria ( Ogura and Hiraga, 1983 ; Hayes and Van Melderen, 2011 ; Fraikin et al, 2020 ; Leroux et al, 2020 ; Kamruzzaman et al, 2021 ; Ni et al, 2021 ; Xue et al, 2022 ). It is worth noting that MGE is closely related to the genetic stability and formation of persisters through horizontal transfer and vertical transmission ( Cooper and Heinemann, 2000 ; Costa et al, 2001 ; Schumacher et al, 2012 , 2015 ; Blair et al, 2015 ; Levin-Reisman et al, 2017 ; Ni et al, 2021 ; Xia et al, 2021 ).…”

“…Followed by the degradation of the corresponding antitoxin partner, the active toxin component was, thus, released to interact with cellular pathways to activate potentially deleterious toxic activities ( Muthuramalingam et al, 2016 ; Leroux et al, 2020 ; Sarpong and Murphy, 2021 ; Xia et al, 2021 ). Furthermore, the type II TAS, which is studied the most and best, is the most abundant in bacterial MGEs among eight TAS types investigated to date ( Xie et al, 2018 ; Kamruzzaman et al, 2021 ; Sarpong and Murphy, 2021 ; Zhang et al, 2021 ; Xue et al, 2022 ). For instance, Ep RatAB and Ep YefM-YoeB TAS from Edwardsiella piscicida are thought to be the model organism for the study of intracellular infections and refer to antibiotic resistance and host infection ( Ma et al, 2021 ; Du et al, 2022 ).…”