Elucidating pathway arsenic methylation
The general efflux detoxification pathway involves the reduction of arsenate to arsenite, and then subsequent expulsion of arsenic from the cell through arsenite-specific transporters (Carlin et al., 1995; Ghosh et al., 1999).
The efflux system, which has evolved independently at least two different times, consists of an arsenate reductase (the analogs Ars C, ACR2 and wzb-like low molecular weight protein tyrosine phosphatase (Bennett et al., 2001)) and an arsenite-specific efflux pump (Ars B or ACR3) (Páez-Espino et al., 2009).
Diagram representing an idealized cross-section of a Prochlorococcus cell highlighting mechanisms likely responsible for arsenic entry into the cell and detoxification.
(1) Arsenate likely enters the cell through the inorganic high affinity phosphate transporters Pst CABS.
The multiple strains of Prochlorococcus possess a variable assortment of accessory genes suited to the specific environments they inhabit (Rocap et al., 2003; Kettler et al., 2007).
The complement of phosphorus acquisition genes in Prochlorococcus also varies among the strains (Martiny et al., 2006).
Prochlorococcus can be divided up into physiologically and genetically distinct ecotypes (Moore et al., 1998) which reflect adaptations to environmental parameters like light intensity (Moore et al., 1998; Moore and Chisholm, 1999), temperature optima (Johnson et al., 2006) and nitrogen utilization capabilities (Moore et al., 2002) among others.
Monomethylarsonic acid (MMA) can undergo a series of oxidation and methylation steps to further methylate the species to dimethylarsinic acid (DMA); further methylation into more compound organoarsenicals may also be possible, but cannot be confirmed without laboratory analysis.
Microbes have evolved multiple mechanisms for cellular defense against arsenic, and the genes involved are taxonomically widespread and subject to frequent horizontal transfer (Stolz et al., 2006; Páez-Espino et al., 2009).
Thus, environmental exposure to arsenic appears to select for maintenance of the efflux detoxification pathway in Prochlorococcus.
The differential distribution of these two pathways has implications for global arsenic cycling, as their associated end products, arsenite or organoarsenicals, have differing biochemical activities and residence times.
Once inside the cell, arsenate can become toxic by competing with phosphate, for example, through the decoupling of oxidative phosphorylation, the process that produces ATP (Mandal and Suzuki, 2002; Oremland and Stolz, 2003).