@article{10768,
  abstract     = {Among the most fascinated properties of the plant hormone auxin is its ability to promote formation of its own directional transport routes. These gradually narrowing auxin channels form from the auxin source toward the sink and involve coordinated, collective polarization of individual cells. Once established, the channels provide positional information, along which new vascular strands form, for example, during organogenesis, regeneration, or leave venation. The main prerequisite of this still mysterious auxin canalization mechanism is a feedback between auxin signaling and its directional transport. This is manifested by auxin-induced re-arrangements of polar, subcellular localization of PIN-FORMED (PIN) auxin exporters. Immanent open questions relate to how position of auxin source and sink as well as tissue context are sensed and translated into tissue polarization and how cells communicate to polarize coordinately. Recently, identification of the first molecular players opens new avenues into molecular studies of this intriguing example of self-organizing plant development.},
  author       = {Hajny, Jakub and Tan, Shutang and Friml, Jiří},
  issn         = {1369-5266},
  journal      = {Current Opinion in Plant Biology},
  number       = {2},
  publisher    = {Elsevier},
  title        = {{Auxin canalization: From speculative models toward molecular players}},
  doi          = {10.1016/j.pbi.2022.102174},
  volume       = {65},
  year         = {2022},
}

@article{8931,
  abstract     = {Auxin is a major plant growth regulator, but current models on auxin perception and signaling cannot explain the whole plethora of auxin effects, in particular those associated with rapid responses. A possible candidate for a component of additional auxin perception mechanisms is the AUXIN BINDING PROTEIN 1 (ABP1), whose function in planta remains unclear.
Here we combined expression analysis with gain- and loss-of-function approaches to analyze the role of ABP1 in plant development. ABP1 shows a broad expression largely overlapping with, but not regulated by, transcriptional auxin response activity. Furthermore, ABP1 activity is not essential for the transcriptional auxin signaling. Genetic in planta analysis revealed that abp1 loss-of-function mutants show largely normal development with minor defects in bolting. On the other hand, ABP1 gain-of-function alleles show a broad range of growth and developmental defects, including root and hypocotyl growth and bending, lateral root and leaf development, bolting, as well as response to heat stress. At the cellular level, ABP1 gain-of-function leads to impaired auxin effect on PIN polar distribution and affects BFA-sensitive PIN intracellular aggregation.
The gain-of-function analysis suggests a broad, but still mechanistically unclear involvement of ABP1 in plant development, possibly masked in abp1 loss-of-function mutants by a functional redundancy.},
  author       = {Gelová, Zuzana and Gallei, Michelle C and Pernisová, Markéta and Brunoud, Géraldine and Zhang, Xixi and Glanc, Matous and Li, Lanxin and Michalko, Jaroslav and Pavlovicova, Zlata and Verstraeten, Inge and Han, Huibin and Hajny, Jakub and Hauschild, Robert and Čovanová, Milada and Zwiewka, Marta and Hörmayer, Lukas and Fendrych, Matyas and Xu, Tongda and Vernoux, Teva and Friml, Jiří},
  issn         = {0168-9452},
  journal      = {Plant Science},
  keywords     = {Agronomy and Crop Science, Plant Science, Genetics, General Medicine},
  publisher    = {Elsevier},
  title        = {{Developmental roles of auxin binding protein 1 in Arabidopsis thaliana}},
  doi          = {10.1016/j.plantsci.2020.110750},
  volume       = {303},
  year         = {2021},
}

@article{8721,
  abstract     = {Spontaneously arising channels that transport the phytohormone auxin provide positional cues for self-organizing aspects of plant development such as flexible vasculature regeneration or its patterning during leaf venation. The auxin canalization hypothesis proposes a feedback between auxin signaling and transport as the underlying mechanism, but molecular players await discovery. We identified part of the machinery that routes auxin transport. The auxin-regulated receptor CAMEL (Canalization-related Auxin-regulated Malectin-type RLK) together with CANAR (Canalization-related Receptor-like kinase) interact with and phosphorylate PIN auxin transporters. camel and canar mutants are impaired in PIN1 subcellular trafficking and auxin-mediated PIN polarization, which macroscopically manifests as defects in leaf venation and vasculature regeneration after wounding. The CAMEL-CANAR receptor complex is part of the auxin feedback that coordinates polarization of individual cells during auxin canalization.},
  author       = {Hajny, Jakub and Prat, Tomas and Rydza, N and Rodriguez Solovey, Lesia and Tan, Shutang and Verstraeten, Inge and Domjan, David and Mazur, E and Smakowska-Luzan, E and Smet, W and Mor, E and Nolf, J and Yang, B and Grunewald, W and Molnar, Gergely and Belkhadir, Y and De Rybel, B and Friml, Jiří},
  issn         = {1095-9203},
  journal      = {Science},
  number       = {6516},
  pages        = {550--557},
  publisher    = {American Association for the Advancement of Science},
  title        = {{Receptor kinase module targets PIN-dependent auxin transport during canalization}},
  doi          = {10.1126/science.aba3178},
  volume       = {370},
  year         = {2020},
}

@phdthesis{8822,
  abstract     = {Self-organization is a hallmark of plant development manifested e.g. by intricate leaf vein patterns, flexible formation of vasculature during organogenesis or its regeneration following wounding. Spontaneously arising channels transporting the phytohormone auxin, created by coordinated polar localizations of PIN-FORMED 1 (PIN1) auxin exporter, provide positional cues for these as well as other plant patterning processes. To find regulators acting downstream of auxin and the TIR1/AFB auxin signaling pathway essential for PIN1 coordinated polarization during auxin canalization, we performed microarray experiments. Besides the known components of general PIN polarity maintenance, such as PID and PIP5K kinases, we identified and characterized a new regulator of auxin canalization, the transcription factor WRKY DNA-BINDING PROTEIN 23 (WRKY23).
Next, we designed a subsequent microarray experiment to further uncover other molecular players, downstream of auxin-TIR1/AFB-WRKY23 involved in the regulation of auxin-mediated PIN repolarization. We identified a novel and crucial part of the molecular machinery underlying auxin canalization. The auxin-regulated malectin-type receptor-like kinase CAMEL and the associated leucine-rich repeat receptor-like kinase CANAR target and directly phosphorylate PIN auxin transporters. camel and canar mutants are impaired in PIN1 subcellular trafficking and auxin-mediated repolarization leading to defects in auxin transport, ultimately to leaf venation and vasculature regeneration defects. Our results describe the CAMEL-CANAR receptor complex, which is required for auxin feed-back on its own transport and thus for coordinated tissue polarization during auxin canalization.},
  author       = {Hajny, Jakub},
  issn         = {2663-337X},
  pages        = {249},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Identification and characterization of the molecular machinery of auxin-dependent canalization during vasculature formation and regeneration}},
  doi          = {10.15479/AT:ISTA:8822},
  year         = {2020},
}

@article{7427,
  abstract     = {Plants, like other multicellular organisms, survive through a delicate balance between growth and defense against pathogens. Salicylic acid (SA) is a major defense signal in plants, and the perception mechanism as well as downstream signaling activating the immune response are known. Here, we identify a parallel SA signaling that mediates growth attenuation. SA directly binds to A subunits of protein phosphatase 2A (PP2A), inhibiting activity of this complex. Among PP2A targets, the PIN2 auxin transporter is hyperphosphorylated in response to SA, leading to changed activity of this important growth regulator. Accordingly, auxin transport and auxin-mediated root development, including growth, gravitropic response, and lateral root organogenesis, are inhibited. This study reveals how SA, besides activating immunity, concomitantly attenuates growth through crosstalk with the auxin distribution network. Further analysis of this dual role of SA and characterization of additional SA-regulated PP2A targets will provide further insights into mechanisms maintaining a balance between growth and defense.},
  author       = {Tan, Shutang and Abas, Melinda F and Verstraeten, Inge and Glanc, Matous and Molnar, Gergely and Hajny, Jakub and Lasák, Pavel and Petřík, Ivan and Russinova, Eugenia and Petrášek, Jan and Novák, Ondřej and Pospíšil, Jiří and Friml, Jiří},
  issn         = {09609822},
  journal      = {Current Biology},
  number       = {3},
  pages        = {381--395.e8},
  publisher    = {Cell Press},
  title        = {{Salicylic acid targets protein phosphatase 2A to attenuate growth in plants}},
  doi          = {10.1016/j.cub.2019.11.058},
  volume       = {30},
  year         = {2020},
}

@article{7500,
  abstract     = {Plant survival depends on vascular tissues, which originate in a self‐organizing manner as strands of cells co‐directionally transporting the plant hormone auxin. The latter phenomenon (also known as auxin canalization) is classically hypothesized to be regulated by auxin itself via the effect of this hormone on the polarity of its own intercellular transport. Correlative observations supported this concept, but molecular insights remain limited.
In the current study, we established an experimental system based on the model Arabidopsis thaliana, which exhibits auxin transport channels and formation of vasculature strands in response to local auxin application.
Our methodology permits the genetic analysis of auxin canalization under controllable experimental conditions. By utilizing this opportunity, we confirmed the dependence of auxin canalization on a PIN‐dependent auxin transport and nuclear, TIR1/AFB‐mediated auxin signaling. We also show that leaf venation and auxin‐mediated PIN repolarization in the root require TIR1/AFB signaling.
Further studies based on this experimental system are likely to yield better understanding of the mechanisms underlying auxin transport polarization in other developmental contexts.},
  author       = {Mazur, E and Kulik, Ivan and Hajny, Jakub and Friml, Jiří},
  issn         = {1469-8137},
  journal      = {New Phytologist},
  number       = {5},
  pages        = {1375--1383},
  publisher    = {Wiley},
  title        = {{Auxin canalization and vascular tissue formation by TIR1/AFB-mediated auxin signaling in arabidopsis}},
  doi          = {10.1111/nph.16446},
  volume       = {226},
  year         = {2020},
}

@article{6260,
  abstract     = {Polar auxin transport plays a pivotal role in plant growth and development. PIN auxin efflux carriers regulate directional auxin movement by establishing local auxin maxima, minima, and gradients that drive multiple developmental processes and responses to environmental signals. Auxin has been proposed to modulate its own transport by regulating subcellular PIN trafficking via processes such as clathrin-mediated PIN endocytosis and constitutive recycling. Here, we further investigated the mechanisms by which auxin affects PIN trafficking by screening auxin analogs and identified pinstatic acid (PISA) as a positive modulator of polar auxin transport in Arabidopsis thaliana. PISA had an auxin-like effect on hypocotyl elongation and adventitious root formation via positive regulation of auxin transport. PISA did not activate SCFTIR1/AFB signaling and yet induced PIN accumulation at the cell surface by inhibiting PIN internalization from the plasma membrane. This work demonstrates PISA to be a promising chemical tool to dissect the regulatory mechanisms behind subcellular PIN trafficking and auxin transport.},
  author       = {Oochi, A and Hajny, Jakub and Fukui, K and Nakao, Y and Gallei, Michelle C and Quareshy, M and Takahashi, K and Kinoshita, T and Harborough, SR and Kepinski, S and Kasahara, H and Napier, RM and Friml, Jiří and Hayashi, KI},
  issn         = {1532-2548},
  journal      = {Plant Physiology},
  number       = {2},
  pages        = {1152--1165},
  publisher    = {ASPB},
  title        = {{Pinstatic acid promotes auxin transport by inhibiting PIN internalization}},
  doi          = {10.1104/pp.19.00201},
  volume       = {180},
  year         = {2019},
}

@article{191,
  abstract     = {Intercellular distribution of the plant hormone auxin largely depends on the polar subcellular distribution of the plasma membrane PIN-FORMED (PIN) auxin transporters. PIN polarity switches in response to different developmental and environmental signals have been shown to redirect auxin fluxes mediating certain developmental responses. PIN phosphorylation at different sites and by different kinases is crucial for PIN function. Here we investigate the role of PIN phosphorylation during gravitropic response. Loss- and gain-of-function mutants in PINOID and related kinases but not in D6PK kinase as well as mutations mimicking constitutive dephosphorylated or phosphorylated status of two clusters of predicted phosphorylation sites partially disrupted PIN3 phosphorylation and caused defects in gravitropic bending in roots and hypocotyls. In particular, they impacted PIN3 polarity rearrangements in response to gravity and during feed-back regulation by auxin itself. Thus PIN phosphorylation, besides regulating transport activity and apical-basal targeting, is also important for the rapid polarity switches in response to environmental and endogenous signals.},
  author       = {Grones, Peter and Abas, Melinda F and Hajny, Jakub and Jones, Angharad and Waidmann, Sascha and Kleine Vehn, Jürgen and Friml, Jirí},
  journal      = {Scientific Reports},
  number       = {1},
  publisher    = {Springer},
  title        = {{PID/WAG-mediated phosphorylation of the Arabidopsis PIN3 auxin transporter mediates polarity switches during gravitropism}},
  doi          = {10.1038/s41598-018-28188-1},
  volume       = {8},
  year         = {2018},
}

@article{449,
  abstract     = {Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17- and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain- and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development.},
  author       = {Prat, Tomas and Hajny, Jakub and Grunewald, Wim and Vasileva, Mina K and Molnar, Gergely and Tejos, Ricardo and Schmid, Markus and Sauer, Michael and Friml, Jirí},
  journal      = {PLoS Genetics},
  number       = {1},
  publisher    = {Public Library of Science},
  title        = {{WRKY23 is a component of the transcriptional network mediating auxin feedback on PIN polarity}},
  doi          = {10.1371/journal.pgen.1007177},
  volume       = {14},
  year         = {2018},
}

