Biology Reference
In-Depth Information
found and one of the most hazardous classes of cyanotoxin. Microcystins are
synthesized in a mixed polyketide synthase/nonribosomal peptide synthe-
tase system called microcystin synthetase. The microcystin synthetase com-
plex in
M. aeruginosa
PCC 7806 is encoded by the
mcy
operon (
Tillett et al.,
2000
). FurA from
M. aeruginosa
recognizes and binds
mcy
promoter regions
(
Martin-Luna et al., 2006
), suggesting a transcriptional control by this global
regulator. Moreover, iron deficiency induces
mcyD
expression, correlating
with higher levels of microcystin in cells (
Sevilla et al., 2008
). Fur and NtcA,
the global nitrate regulator, balance iron, carbon and nitrogen metabolism
resulting in a fine control of the expression of the microcystin gene cluster
(
Kuniyoshi et al., 2011
).
In heterotrophic bacteria, Fur regulates peptide synthetase systems
involved in the synthesis of virulence factors, such as enterobactin and
vibriobactin, among others (
Crosa & Walsh, 2002
). These nonribosomal
peptide synthetases are similar to the enzymes involved in the synthesis
of microcystins. Many of these toxins are siderophores, and even though
the ecostrategy or physiological meaning of microcystin production is
unknown, several observations suggest a link between microcystin produc-
tion and iron metabolism. During iron depletion, toxic strains of
Microcystis
maintained cell vitality much longer than nontoxic strains (
Lyck, Gjølme, &
Utkilen, 1996
). Moreover, the rate of iron uptake in toxic strains was higher
than nontoxic strains (
Utkilen & Gjolme, 1995
). Comparison between the
iron-stress response in toxic and nontoxic strains of
M. aeruginosa
reveals that
the adaptation of
Microcystis
to iron stress is highly dynamic and strain spe-
cific (
Alexova et al., 2011
). The ability to produce microcystin seems to give
an advantage to toxic cyanobacteria in the early stages of exposure to severe
iron stress and may protect the cell from reactive oxygen species-induced
damage. All those observations strongly support that microcystin produc-
tion may be a FurA-controlled physiological response to iron deficiency.
In summary, these connections strongly suggest that Fur proteins play a
central role in the adaptation of cyanobacteria to different environmental
and nutritional stresses.
3.2. Regulation of Iron-Sulphur Cluster Assembly
Iron-sulphur clusters display versatile functions including stabilization of
protein structure, gene regulation, environmental sensing and radical gen-
eration (
Johnson, 1998
). Because of their sensitivity to cellular redox status,
iron-sulphur clusters are considered as molecular switches for gene regula-
tion at both the transcriptional and translational levels (
Kiley & Beinert,
