Abstract
Prokaryotic tolerance to inorganic arsenic is a widespread trait habitually determined by operons encoding an As (III)-responsive repressor (ArsR), an As (V)-reductase (ArsC), and an As (III)-export pump (ArsB), often accompanied by other complementary genes. Enigmatically, the genomes of many environmental bacteria typically contain two or more copies of this basic genetic device arsRBC. To shed some light on the logic of such apparently unnecessary duplication(s) we have inspected the regulation—together and by separate—of the two ars clusters borne by the soil bacterium Pseudomonas putida strain KT2440, in particular the cross talk between the two repressors ArsR1/ArsR2 and the respective promoters. DNase I footprinting and gel retardation analyses of Pars1 and Pars2 with their matching regulators revealed non-identical binding sequences and interaction patterns for each of the systems. However, in vitro transcription experiments exposed that the repressors could downregulate each other’s promoters, albeit within a different set of parameters. The regulatory frame that emerges from these data corresponds to a particular type of bifan motif where all key interactions have a negative sign. The distinct regulatory architecture that stems from coexistence of various ArsR variants in the same cells could enter an adaptive advantage that favors the maintenance of the two proteins as separate repressors.
Highlights
Various chemical species of arsenic pollute soil and water of many countries and cause serious environmental and health issues (Rosen, 1971; Páez-Espino et al, 2009) in a fashion that depends on the chemical species (+V, +III, 0, −III; Rosen, 2002; Oremland and Stolz, 2003)
The regulatory architecture of both Pars1 and Pars2 promoters is identical and somewhat odd, as it involves self-repression of the repressor (Figure 1A), an arrangement that depending on parameters often causes strong stochastic effects when the actors are in a repression mode (Alon, 2019)
While the maintenance of twin arsenic resistance operons has been explained both as a case of ecoparalogy (Páez-Espino et al, 2015) and/or synergistic collaboration to reach a high tolerance to the oxyanion, the efficient interplay of ArsR1 and ArsR2 with their non-cognate promoters remains puzzling
Summary
Various chemical species of arsenic pollute soil and water of many countries and cause serious environmental and health issues (Rosen, 1971; Páez-Espino et al, 2009) in a fashion that depends on the chemical species (+V, +III, 0, −III; Rosen, 2002; Oremland and Stolz, 2003). It is possible to find more genes in the ars operon depending on the bacterial species (arsA, arsD, arsH, and others; Suzuki et al, 1997, 1998; Silver, 1998; Páez-Espino et al, 2020) the most conserved are the three cited above. Genes encoding ArsR proteins belong to the family of ArsR-SmtB sensors, a widespread group of transcriptional factors characterized by the ability to respond to arsenic, antimony and bismuth. These regulators embody two distinct domains i.e., a DNA binding segment with a typical helix-turn-helix motif (HTH; Barbosa et al, 2007), and a ligand-docking amino acid sequence with a α3 helix signature, capable of binding arsenite (Busenlehner et al, 2003)
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