Biology Reference
In-Depth Information
transcriptional regulator with NO. Similarly, this remains a speculative
hypothesis and will require experimental verification.
7.6. NO resistance in oxygen-limited conditions
An adaptive response to nitrosative stress that is independent of NssR, Cgb
or NrfA has been suggested under oxygen-limited conditions (
Avila-
Ramirez et al., 2013
). Under microaerobic conditions, NssR-dependent
Cgb induction in cultures pre-treated with GSNO protects
C. jejuni
respi-
ration from NO inhibition (
Avila-Ramirez et al., 2013; Elvers et al., 2004
).
However, under conditions of oxygen limitation, GSNO pre-treatment
produces a more modest, yet significant, decrease in NO-mediated inhibi-
tion of respiration (
Avila-Ramirez et al., 2013
) compared to untreated cells.
As this protection proved to be independent of NssR, an inducible NO
detoxification system, unrelated to either members of the NssR regulon
or NrfA, seems to be playing a role. This putative system remains to be
characterised, yet may be of importance during
Campylobacter
infection,
where oxygen tension is known to be extremely low.
8. INTEGRATED RESPONSE INVOLVING CGB AND CTB
Direct interplay between haemoglobins co-existing in the same
microorganism has not been reported. However, given that
cgb
and
ctb
are members of the same regulon, their upregulation is linked to nitrosative
stress (via NssR) and considering the role of Ctb under these conditions is
not obvious (
Elvers et al., 2005
), an integrated response involving Cgb and
Ctb is possible.
Elevated expression of Cgb in a
ctb
mutant was recently reported under
oxygen-limited conditions (
Smith et al., 2011
). This finding lead to specu-
lation that Ctb modulates the availability of NO and, as a consequence, con-
trols NssR activity. This phenomenon was observed under microaerobic
conditions, where the haem cofactor of Ctb exists in an oxyferrous form
(
Wainwright et al., 2006
), and the binding of NO to the ferrous iron of
Ctb is therefore likely to be hindered. This suggests that when nitrosative
stress is encountered under microaerobic conditions, NssR is activated
by the available NO. However, when the oxygen concentration is limited,
the unliganded ferrous haem of Ctb binds NO and consequently prevents
the induction of Cgb (
Smith et al., 2011
). The failure of NO-exposed cells
