High impact information on EIR1

• Taken together, these data suggest that the EIR1 protein has a root-specific role in the transport of auxin [1].
• EIR1, a root-specific protein involved in auxin transport, is required for gravitropism in Arabidopsis thaliana [1].
• The EIR1 gene of Arabidopsis is a member of a family of plant genes with similarities to bacterial membrane transporters [1].
• This gene is expressed only in the root, which is consistent with the phenotypes of the eir1 mutants-the roots are agravitropic and have a reduced sensitivity to ethylene [1].
• Intracellular trafficking and proteolysis of the Arabidopsis auxin-efflux facilitator PIN2 are involved in root gravitropism [2].

Biological context of EIR1

• In contrast, the rhd1-4 short root and root epidermal bulging phenotypes did not require EIN2, EIN3, or EIR1 [3].
• We have isolated an Arabidopsis mutant of the AtPIN2 gene using transposon mutagenesis [4].
• The AtPIN2 gene consists of nine exons defining an open reading frame of 1944 bp which encodes a 69 kDa protein with 10 putative transmembrane domains interrupted by a central hydrophilic loop [4].
• The AtPIN2 gene was mapped to chromosome 5 (115.3 cM) corresponding to the WAV6 locus and subsequent genetic analysis indicated that wav6-52 and Atpin2::En701 were allelic [4].
• We used positional cloning to show that AGR1 encodes a putative transmembrane protein whose amino acid sequence shares homologies with bacterial transporters [5].

Anatomical context of EIR1

• In root cells, we further show that AtSNX1 localizes to an endosomal compartment distinct from GNOM-containing endosomes, and that PIN2 accumulates in this compartment after treatment with the phosphatidylinositol-3-OH kinase inhibitor wortmannin or after a gravity stimulus [6].
• The AtPIN2 protein was localized in membranes of root cortical and epidermal cells in the meristematic and elongation zones revealing a polar localization [4].
• Ultrastructure and movements of cell organelles in the root cap of agravitropic mutants and normal seedlings of Arabidopsis thaliana [7].

Associations of EIR1 with chemical compounds

• In the present study, double mutant analyses revealed that only rhd1-4 hypersusceptibility to H. schachtii and increased root hair elongation were dependent upon the ethylene signaling genes EIN2 and EIN3 but not upon ethylene signaling mediated by the auxin efflux carrier EIR1 [3].
• Sensitivity to jasmonic acid and functional NPR1 and EIR1 proteins were required for full expression of CHA0r-mediated ISR [8].
• Complex regulation of Arabidopsis AGR1/PIN2-mediated root gravitropic response and basipetal auxin transport by cantharidin-sensitive protein phosphatases [9].
• Constitutive overexpression of ROP2 results in enhanced polar accumulation of PIN2 protein in the root elongation region and increased gravitropism, which is significantly affected by latrunculin B, an inhibitor of F-actin assembly [10].
• BFA causes coaccumulation of sterols, endocytic markers like ARA6-GFP, and PIN2, a polarly localized presumptive auxin transport protein, in early endosome agglomerations that can be distinguished from ER and Golgi [11].

Other interactions of EIR1

• Here we show that Arabidopsis thaliana SORTING NEXIN 1 (AtSNX1) is involved in the auxin pathway and that PIN2, but not PIN1 or AUX1, is transported through AtSNX1-containing endosomes [6].
• The EIR1, AUX1 and HLS1 genes may function in the interactions between ethylene and other plant hormones that occur late in the signaling pathway of this simple gas [12].
• We have identified several AGR1-related genes in Arabidopsis, suggesting a global role of this gene family in the control of auxin-regulated growth and developmental processes [5].
• However, inhibition of hypocotyl elongation by FR, induction of cotyledon unfolding, and induction of agravitropic growth were not affected by loss of phytochrome E [13].
• At low fluence rates of blue light phot1 mutants were agravitropic [14].

Analytical, diagnostic and therapeutic context of EIR1

• Complementation tests indicate that rgr1 is not allelic to previously characterized agravitropic or auxin-resistant mutants [15].

References