Abstract
To clarify the roles of carbon monoxide (CO), nitric oxide (NO), and auxin in the plant response to iron deficiency (–Fe), and to establish how the signaling molecules interact to enhance Fe acquisition, we conducted physiological, genetic, and molecular analyses that compared the responses of various
Arabidopsis
mutants, including
hy1
(CO deficient),
noa1
(NO deficient),
nia1/nia2
(NO deficient),
yuc1
(auxin over-accumulation), and
cue1
(NO over-accumulation) to –Fe stress. We also generated a HY1 over-expression line (named HY1-OX) in which CO is over-produced compared to wild-type. We found that the suppression of CO and NO generation using various inhibitors enhanced the sensitivity of wild-type plants to Fe depletion. Similarly, the
hy1
,
noa1
, and
nia1
/
nia2
mutants were more sensitive to Fe deficiency. By contrast, the
yuc1
,
cue1
, and HY1-OX lines were less sensitive to Fe depletion. The
hy1
mutant with low CO content exhibited no induced expression of the Fe uptake-related genes
FIT1
and
FRO2
as compared to wild-type plants. On the other hand, the treatments of exogenous CO and NO enhanced Fe uptake. Likewise,
cue1
and HY1-OX lines with increased endogenous content of NO and CO, respectively, also exhibited enhanced Fe uptake and increased expression of bHLH transcriptional factor FIT1as compared to wild-type plants. Furthermore, we found that CO affected auxin accumulation and transport in the root tip by altering the PIN1 and PIN2 proteins distribution that control lateral root structure under –Fe stress. Our results demonstrated the integration of CO, NO, and auxin signaling to cope with Fe deficiency in
Arabidopsis
.