High impact information on PIN1

• PIN1 polar localization undergoes a dynamic rearrangement, which correlates with establishment of auxin gradients and primordium development [1].
• In this issue of Cell, Geldner et al. demonstrate that the Arabidopsis ARF activator GNOM localizes to endosomes where it controls the polarized trafficking of the auxin efflux carrier PIN1 to the basal plasma membrane [2].
• Both PIN1 localization and auxin transport are also sensitive to BFA [3].
• The Arabidopsis protein GNOM is a brefeldin A (BFA) sensitive ARF-GEF that is required for the proper polar localization of PIN1, a candidate transporter of the plant hormone auxin [3].
• Asymmetric localization of PIN1 develops from a random distribution in Arabidopsis early embryogenesis [4].

Biological context of PIN1

• This phenotype, combined with the proposed role of PIN1 in hormone transport, makes the mutant an ideal tool to study organ formation and phyllotaxis, and here we present a detailed analysis of the molecular modifications at the shoot apex caused by the mutation [5].
• Conversely, pid loss of function induces an apical-to-basal shift in PIN1 polar targeting at the inflorescence apex, accompanied by defective organogenesis [6].
• Our results suggest a model where PIN1 and MP regulate apical patterning partially through the control of CUC gene expression [7].
• Hydathodes, which develop in the tip and later in the lobes, were apparently primary sites of high free-auxin production, the latter supported by auxin-conjugate hydrolysis, auxin retention by the chalcone synthase-dependent action of flavonoids and also by the PIN1-component of the carrier-mediated basipetal transport [8].
• Enhanced gravi- and phototropism in plant mdr mutants mislocalizing the auxin efflux protein PIN1 [9].

Anatomical context of PIN1

• Apical and basal plasma membrane localization of AUXIN-RESISTANT1 (AUX1) and PIN-FORMED1 (PIN1) auxin transport components underpins the directionality of intercellular auxin flow in Arabidopsis thaliana roots [10].
• Overexpression of PID (PIDox) or the auxin efflux carrier component PINFORMED3 (PIN3, PIN3ox), specifically in the root hair cell, greatly suppressed root hair growth [11].
• 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 [12].

Associations of PIN1 with chemical compounds

• Subcellular Trafficking of the Arabidopsis Auxin Influx Carrier AUX1 Uses a Novel Pathway Distinct from PIN1 [10].
• We found normal PIN1:GFP localization at the apical membrane of root cells, but treatment with brefeldin A resulted in PIN1 accumulating in smaller and more numerous compartments than in the wild type [13].

Regulatory relationships of PIN1

• We found evidence that MP expression can be activated by auxin exposure and that PIN1 as well as DR5::GUS expression is defective in mp mutant leaves [14].

Other interactions of PIN1

• This strongly suggests that ENP specifically regulates cotyledon development through control of PIN1 polarity in concert with PID [15].
• Taken together the results suggest a feedback regulatory loop that involves auxin, MP and PIN1 and provide novel experimental support for the canalization-of-auxin-flow hypothesis [14].
• Chemical and genetic inhibition revealed that auxin transport activity, in particular that of the PIN-FORMED1 (PIN1) and PIN4 proteins, is a major factor in the maintenance of these gradients [16].
• Later, the developmentally regulated reversal of PIN7 and onset of PIN1 polar localization reorganize the auxin gradient for specification of the basal root pole [17].
• Chemical inhibition of polar auxin transport (PAT) severely affects the apical-basal patterning of the gynoecium, as do mutations in the auxin transport/signalling genes PIN1, PID and ETT [18].

Analytical, diagnostic and therapeutic context of PIN1

• To determine whether PIN1 intracellular trafficking was affected, we analyzed PIN1:green fluorescent protein (GFP) dynamics using confocal microscopy in sfc roots [13].

References