Together with ABCG37, regulates auxin homeostasis and responses by playing a dual role in coumarine (e.g. esculin) and in the auxin precursor indole 3-butyric acid (IBA) efflux transport, thus influencing cotyledons, roots and root hairs development. Mediates the transport (export into the apoplast) of distinct indole-type metabolites in distinct biological processes; a precursor of 4-O-beta-D-glucosyl-indol-3-yl formamide (4OGlcI3F), a pathogen-inducible tryptophan-derived compound (e.g. upon Blumeria graminis conidiospore inoculation), being a probable substrate in extracellular pathogen defense. Involved in the cellular detoxification of xenobiotics by promoting the excretion of some auxinic herbicides including 4-(2,4-dichlorophenoxy)butyric acid (2,4-DB) and other members of the phenoxyalkanoic acid family but not 2,4-dichlorophenoxyacetic acid (2,4-D). Mediates thymidine exudation in the rhizosphere. May be a transporter of lignin precursors during tracheary element differentiation. Key factor that controls the extent of cell death in the defense response. Necessary for both callose deposition and glucosinolate activation in response to pathogens. As a central component of nonhost resistance (NHR), required for limiting invasion by nonadapted pathogens including powdery mildews (e.g. Blumeria graminis and Erysiphe pisi), root-penetrating pathogenic fungi (e.g. Fusarium oxysporum), Phakopsora pachyrhizi and Colletotrichum gloeosporioides (anthracnose fungi), probably by sensing Ca(2+) via interactions with calmodulins (e.g. CaM7). Confers resistance to cadmium (Cd) and lead (Pb), probably as an efflux pump of Cd2+ or Cd conjugates, and possibly, of chemicals that mediate pathogen resistance. Promotes resistance to abiotic stresses (e.g. drought and salt stress) and favors general growth by preventing sodium accumulation in plants. Required for microbe-associated molecular patterns (MAMPs)- and salicylic acid (SA)-dependent hypersensitive cell death (HR), involving indole glucosinolate breakdown products (e.g. indole-3-acetonitrile), probably in a PEN2 myrosinase-dependent metabolic pathway, triggered by the recognition of effectors from incompatible pathogens including oomycetes and bacteria (e.g. AvrRpm1 and AvrRps4) and benzothiadiazole- (BTH), and leading to an induced protection against pathogens (e.g. Pseudomonas syringae pv. tomato DC3000, Golovinomyces orontii and Hyaloperonospora arabidopsidis).
