Differential distribution of the plant hormone auxin within tissues mediates a variety of developmental processes. Cellular auxin levels are determined by metabolic processes including synthesis, degradation, and (de)conjugation, as well as by auxin transport across the plasma membrane. Whereas transport of free auxins such as naturally occurring indole-3-acetic acid (IAA) is well characterized, little is known about the transport of auxin precursors and metabolites. Here, we identify a mutation in the ABCG37 gene of Arabidopsis that causes the polar auxin transport inhibitor sensitive1 (pis1) phenotype manifested by hypersensitivity to auxinic compounds. ABCG37 encodes the pleiotropic drug resistance transporter that transports a range of synthetic auxinic compounds as well as the endogenous auxin precursor indole-3-butyric acid (IBA), but not free IAA. ABCG37 and its homolog ABCG36 act redundantly at outermost root plasma membranes and, unlike established IAA transporters from the PIN and ABCB families, transport IBA out of the cells. Our findings explore possible novel modes of regulating auxin homeostasis and plant development by means of directional transport of the auxin precursor IBA and presumably also other auxin metabolites.PDR9 | PDR8 | IBA transport | auxin synthesis P lants have evolved outstanding capacities to adapt their metabolism and development to respond to their environment. Changes in the availability and distribution of endogenous signaling molecules-plant hormones-play important roles in these responses (1). The phytohormone auxin, perceived by TIR1/AFB receptor proteins and interpreted by downstream nuclear signaling pathway, is an important signal that mediates transcriptional developmental reprogramming (reviewed in refs. 2 and 3). The differential distribution of auxin within tissues is essential for many adaptive responses including embryo and leaf patterning, root and stem elongation, lateral root initiation, and leaf expansion (4). Differential distribution of the major active auxin, IAA, depends on its intercellular transport and metabolic processes that involve biosynthesis by several pathways and release from storage forms including amide-or ester-linked conjugates with amino acids, peptides, and sugars (reviewed in ref. 5). The role of another endogenously occurring auxinic compound IBA is still unclear. It has been proposed that IBA acts independently of IAA (6), but a number of recent genetic findings suggest that IBA functions as an important precursor to IAA during conversion resembling peroxisomal fatty acid β-oxidation (5, 7). Besides metabolism, a crucial process controlling cellular auxin levels is the directional, intercellular auxin transport that depends on specialized influx and efflux carriers (reviewed in ref. 8). IAA transporters include amino acid permeases-like AUXIN RESISTANT1 (AUX1) mediating auxin influx (9-11), the PIN-FORMED (PIN) efflux carriers (12)(13)(14), and the MULTIDRUG RESISTANCE/P-GLYCOPROTEIN (PGP) class of ATP-Binding Cassette (ABC) auxin trans...

Synechocystis: sp. PCC 6803 is a unicellular motile cyanobacterium, which shows positive or negative phototaxis on agar plates under lateral illumination. By gene disruption in a substrain showing of positive phototaxis, it was demonstrated that mutants defective in sll0038, sll0039, sll0041, sll0042 or sll0043 lost positive phototaxis but showed negative phototaxis away from the light source. Mutants of sll0040, which is located within the cluster of these genes, retained the capacity of positive phototaxis but to a lesser extent than the parent cells. These genes are homologous to che genes, which are involved in flagellar switching for bacterial chemotaxis. Interestingly, sll0041 (designated pisJ1) is predicted to have a chromophore-binding motif of phytochrome-like proteins and a signaling motif of chemoreceptors for bacterial chemotaxis. It is strongly suggested that the positive phototactic response was mediated by a phytochrome-like photoreceptor and CheA/CheY-type signal transduction system.

Stomata, valves on the plant epidermis, are critical for plant growth and survival, and the presence of stomata impacts the global water and carbon cycle. Although transcription factors and cell-cell signaling components regulating stomatal development have been identified, it remains unclear as to how their regulatory interactions are translated into two-dimensional patterns of stomatal initial cells. Using molecular genetics, imaging, and mathematical simulation, we report a regulatory circuit that initiates the stomatal cell-lineage. The circuit includes a positive feedback loop constituting self-activation of SCREAMs that requires SPEECHLESS. This transcription factor module directly binds to the promoters and activates a secreted signal, EPIDERMAL PATTERNING FACTOR2, and the receptor modifier TOO MANY MOUTHS, while the receptor ERECTA lies outside of this module. This in turn inhibits SPCH, and hence SCRMs, thus constituting a negative feedback loop. Our mathematical model accurately predicts all known stomatal phenotypes with the inclusion of two additional components to the circuit: an EPF2-independent negative-feedback loop and a signal that lies outside of the SPCH•SCRM module. Our work reveals the intricate molecular framework governing self-organizing two-dimensional patterning in the plant epidermis.