(Sakaguchi and Nakajima 1991). Quite the opposite, the occurrence of Fe
2+ and
Zn
2+ affects the uptake of uranium through Rhizopus arrhizus (Tsezos and
Volesky 1982), while cobalt uptake by various microorganisms is totally banned
by the presence of uranium, lead, mercury and copper (Sakaguchi and Nakajima
1991; Elen Aquino Perpetuo et al. 2011).
12.7 Diversity of Metal-Resistant Genes and Biotechniques
in Metal-Resistant Bacteria for Bioremediation
Microorganisms have developed methods to tolerate harmful natural compounds in
the polluted environment and remediate them for their own profit (Guo et al. 2010).
The capacity of bacteria to oppose toxic metals is because of highly modified genetic
systems, through which they synthesize proteins and make it possible to flourish in
the presence of these elements. Bacteria continue to exist due to induction of various
metal-tolerant genes for harmful metals like cadmium, chromium, copper, lead,
mercury and nickel. They can live in an extremely toxic environment because of
these tolerant genes which are employed further for bioremediation. The objective of
the selecting metal is the comparative plentiness of these metal pollutants in the
surroundings and their toxicity level as specified by USEPA and the US Department
of Labor (https://www.osha.gov/SLTC/metalsheavy/). Bacteria have their own
defence mechanisms which develop a tolerance for these harmful metals and may
be utilized to clean-up the polluted environments. Cadmium is an extremely toxic
non-essential metal which can be very dangerous even in very small concentrations.
According to the first report on cadmium genetics, no special cadmium resistance
method is present in bacteria (Silver and Misra 1984). However, it was extensively
opposed by Trevors et al. (1986) as he investigated cadmium transport, tolerance and
toxicity in bacteria, algae and fungi. Tolerance to cadmium is due to cad operon of
plasmid found in Staphylococcus spp. as well as by czc operon at 3972-bp element
of P. aeruginosa (Crupper et al. 1999; Chakraborty and Das 2014). cadA and cadB
operons are parts of cad operon (Zhang et al. 2015), while two genes, cadA and
cadC, are constituent of cadA operon present in plasmid pI258 (Nucifora et al.
1989). CadA protein has homology with ArsB protein of the ars operon and forms an
energy-dependent ATPase which effluxes cadmium from the bacterial cell to give
protection. CadC protein is the transcriptional regulator of the operon (Hsieh et al.
2010). A 204-residue polypeptide is encoded by the cadB operon whose mechanism
of action is still not totally known. It is presumed that cadB, present on the plasmid
pII147 cellularly, binds cadmium, most probably at the plasma membrane (Smith
and Novick 1972). According to Crupper et al. (1999), another novel cadmium
tolerance process is present in the plasmid pRW001 of Staphylococcus aureus which
is due to the presence of cadD system with its two genes, cadD and cadX*. cadD is
similar to the gene cadB, while cadX* is encoding an inactive transcription regulator. However, this operon imparts only low cadmium tolerance. According to
Chaouni et al. (1996), another cadmium-tolerant operon is present in the plasmid
pLUG10 of S. lugdunensis which had a cadB-like gene for tolerance and another
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