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A Golgi-localized MATE transporter mediates iron homoeostasis under osmotic stress in Arabidopsis

Cited 35 time in Web of Science Cited 34 time in Scopus
Authors
Seo, Pil Joon; Park, Jungmin; Park, Mi-Jeong; Kim, Youn-Sung; Kim, Sang-Gyu; Jung, Jae-Hoon; Park, Chung-Mo
Issue Date
2012-03
Citation
Biochemical Journal, Vol.442, pp.551-561
Keywords
abiotic stressArabidopsisiron homoeostasismultidrug and toxic compound extrusion (MATE) transportersenescence
Abstract
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 bcd 1-1. 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.
ISSN
0264-6021
URI
https://hdl.handle.net/10371/171967
DOI
https://doi.org/10.1042/BJ20111311
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College of Natural Sciences (자연과학대학)Dept. of Chemistry (화학부)Journal Papers (저널논문_화학부)
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