Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0240066 (
iron deficiency
)
7,156
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Iron is an essential micronutrient that acts as a cofactor in a wide variety of pivotal metabolic processes, such as the electron transport chain of respiration, photosynthesis and redox reactions, in plants. However, its overload exceeding the cellular capacity of iron binding and storage is potentially toxic to plant cells by causing oxidative stress and cell death. Consequently, plants have developed versatile mechanisms to maintain iron homoeostasis. Organismal iron content is tightly regulated at the steps of uptake, translocation and compartmentalization. Whereas iron uptake is fairly well understood at the cellular and organismal levels, intracellular and intercellular transport is only poorly understood. In the present study, we show that a MATE (multidrug and toxic compound extrusion) transporter, designated
BCD1
(BUSH-AND-CHLOROTIC-DWARF 1), contributes to iron homoeostasis during stress responses and senescence in Arabidopsis. The
BCD1
gene is induced by excessive iron, but repressed by
iron deficiency
. It is also induced by cellular and tissue damage occurring under osmotic stress. The activation-tagged mutant bcd1-1D exhibits leaf chlorosis, a typical symptom of
iron deficiency
. The chlorotic lesion of the mutant was partially recovered by iron feeding. Whereas the bcd1-1D mutant accumulated a lower amount of iron, the iron level was elevated in the knockout mutant bcd1-1. The
BCD1
protein is localized to the Golgi complex. We propose that the
BCD1
transporter plays a role in sustaining iron homoeostasis by reallocating excess iron released from stress-induced cellular damage.
...
PMID:A Golgi-localized MATE transporter mediates iron homoeostasis under osmotic stress in Arabidopsis. 2215 Jan 60