摘要
Arsenic contamination is a major environmental issue,as it may lead to serious health hazard.The reduced trivalent formof inorganic arsenic,arsenite,is in generalmore toxic to plants comparedwith the fully oxidized pentavalent arsenate.Theuptakeof arsenite inplants hasbeenshown tobemediatedthrough a large subfamily of plant aquaglyceroporins,nodulin 26-like intrinsic proteins(NIPs).However,the efflux mechanisms,as well as themechanismof arsenite-induced root growth inhibition,remain poorly understood.Usingmolecular physiology,synchrotron imaging,and root transport assay approaches,we show that the cellular transport of trivalent arsenicals inArabidopsis thalianais stronglymodulatedbyPINFORMED2(PIN2)auxin efflux transporter.Root transport assay using radioactive arsenite,X-ray fluorescence imaging(XFI)coupled with X-ray absorption spectroscopy(XAS),and inductively coupled plasma mass spectrometry analysis revealed that pin2 plants accumulate higher concentrations of arsenite in roots comparedwith the wild-type.At the cellular level,arsenite specifically targets intracellular sorting of PIN2 and thereby alters the cellular auxin homeostasis.Consistently,loss of PIN2 function results in arsenite hypersensitivity in roots.XFI coupled with XAS further revealed that loss of PIN2 function results in specific accumulation of arsenical species,but not the other metals such as iron,zinc,or calcium in the root tip.Collectively,these results suggest that PIN2 likely functions as an arsenite efflux transporter for the distribution of arsenical species in planta.
基金
supported in part by the Iwate University President Fund(to A.R.)
Global Innovation Fund,University of Saskatchewan(to I.P.,G.N.G.,and A.R.)
supported by grants from the Natural Sciences and Engineering Research Council of Canada(G.N.G.,I.P.)
the Saskatchewan Health Research Foundation(G.N.G.,I.P.)
The University of Saskatchewan,and Canada Research Chairs(G.N.G.,I.P.)
supported by the US Department of Energy(DOE)Office of Science User Facility operated for the DOE Office of Science by Argonne National Laboratory under contract no.DE-AC02-06CH11357
supported by the US DOE,Office of Science,Office of Basic Energy Sciences under contract no.DE-AC02-76SF00515
supported by the DOE Office of Biological and Environmental Research
by the National Institutes of Health(NIH)
National Institute of General Medical Sciences(NIGMS)(including P41GM103393)。
