Iron (Fe) is an essential microelement but is highly toxic when in excess. The response of plant roots to Fe toxicity and the nature of the regulatory pathways engaged are poorly understood. Here, we examined the response to excess Fe exposure in Arabidopsis wild type and ethylene mutants with a focus on primary root growth and the role of ethylene. We showed that excess Fe arrested primary root growth by decreasing both cell elongation and division, and principally resulteds from direct external Fe contact at the root tip. Pronounced ethylene, but not abscisic acid, evolution was associated with excess Fe exposure. Ethylene antagonists intensified root growth inhibition in the wild type, while the inhibition was significantly reduced in ethylene-overproduction mutants. We showed that ethylene plays a positive role in tissue Fe homeostasis, even in the absence of iron-plaque formation. Ethylene reduced Fe concentrations in the stele, xylem, and shoot. Furthermore, ethylene increased the expression of genes encoding Fe-sequestering ferritins. Additionally, ethylene significantly enhanced root K(+) status and upregulated K(+)-transporter (HAK5) expression. Our findings highlight the important role of ethylene in tissue Fe and K homeostasis and primary root growth under Fe stress in Arabidopsis.
Keywords: Arabidopsis; Fe homeostasis; Fe toxicity; ethylene; primary root growth..
© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.