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Phosphate starvation response controls genes required to synthesize the phosphate analog arsenate
Author(s) -
Wang Qian,
Kang YoonSuk,
Alowaifeer Abdullah,
Shi Kaixiang,
Fan Xia,
Wang Lu,
Jetter Jonathan,
Bothner Brian,
Wang Gejiao,
McDermott Timothy R.
Publication year - 2018
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.14108
Subject(s) - arsenite , arsenate , phosphate , arsenic , biology , biochemistry , arsenic toxicity , signal transduction , chemistry , organic chemistry
Summary Environmental arsenic poisoning affects roughly 200 million people worldwide. The toxicity and mobility of arsenic in the environment is significantly influenced by microbial redox reactions, with arsenite (As III ) being more toxic than arsenate (As V ). Microbial oxidation of As III to As V is known to be regulated by the AioXSR signal transduction system and viewed to function for detoxification or energy generation. Here, we show that As III oxidation is ultimately regulated by the phosphate starvation response (PSR), requiring the sensor kinase PhoR for expression of the As III oxidase structural genes aioBA . The PhoRB and AioSR signal transduction systems are capable of transphosphorylation cross‐talk, closely integrating As III oxidation with the PSR. Further, under PSR conditions, As V significantly extends bacterial growth and accumulates in the lipid fraction to the apparent exclusion of phosphorus. This could spare phosphorus for nucleic acid synthesis or triphosphate metabolism wherein unstable arsenic esters are not tolerated, thereby enhancing cell survival potential. We conclude that As III oxidation is logically part of the bacterial PSR, enabling the synthesis of the phosphate analog As V to replace phosphorus in specific biomolecules or to synthesize other molecules capable of a similar function, although not for total replacement of cellular phosphate.