@article{10583,
  abstract     = {The synthetic strigolactone (SL) analog, rac-GR24, has been instrumental in studying the role of SLs as well as karrikins because it activates the receptors DWARF14 (D14) and KARRIKIN INSENSITIVE 2 (KAI2) of their signaling pathways, respectively. Treatment with rac-GR24 modifies the root architecture at different levels, such as decreasing the lateral root density (LRD), while promoting root hair elongation or flavonol accumulation. Previously, we have shown that the flavonol biosynthesis is transcriptionally activated in the root by rac-GR24 treatment, but, thus far, the molecular players involved in that response have remained unknown. To get an in-depth insight into the changes that occur after the compound is perceived by the roots, we compared the root transcriptomes of the wild type and the more axillary growth2 (max2) mutant, affected in both SL and karrikin signaling pathways, with and without rac-GR24 treatment. Quantitative reverse transcription (qRT)-PCR, reporter line analysis and mutant phenotyping indicated that the flavonol response and the root hair elongation are controlled by the ELONGATED HYPOCOTYL 5 (HY5) and MYB12 transcription factors, but HY5, in contrast to MYB12, affects the LRD as well. Furthermore, we identified the transcription factors TARGET OF MONOPTEROS 5 (TMO5) and TMO5 LIKE1 as negative and the Mediator complex as positive regulators of the rac-GR24 effect on LRD. Altogether, hereby, we get closer toward understanding the molecular mechanisms that underlay the rac-GR24 responses in the root.},
  author       = {Struk, Sylwia and Braem, Lukas and Matthys, Cedrick and Walton, Alan and Vangheluwe, Nick and Van Praet, Stan and Jiang, Lingxiang and Baster, Pawel and De Cuyper, Carolien and Boyer, Francois-Didier and Stes, Elisabeth and Beeckman, Tom and Friml, Jiří and Gevaert, Kris and Goormachtig, Sofie},
  issn         = {1471-9053},
  journal      = {Plant & Cell Physiology},
  keywords     = {flavonols, MAX2, rac-Gr24, RNA-seq, root development, transcriptional regulation},
  number       = {1},
  pages        = {104--119},
  publisher    = {Oxford University Press},
  title        = {{Transcriptional analysis in the Arabidopsis roots reveals new regulators that link rac-GR24 treatment with changes in flavonol accumulation, root hair elongation and lateral root density}},
  doi          = {10.1093/pcp/pcab149},
  volume       = {63},
  year         = {2022},
}

@article{6104,
  abstract     = {Abiotic stress poses constant challenges for plant survival and is a serious problem for global agricultural productivity. On a molecular level, stress conditions result in elevation of reactive oxygen species (ROS) production causing oxidative stress associated with oxidation of proteins and nucleic acids as well as impairment of membrane functions. Adaptation of root growth to ROS accumulation is facilitated through modification of auxin and cytokinin hormone homeostasis. Here, we report that in Arabidopsis root meristem, ROS-induced changes of auxin levels correspond to decreased abundance of PIN auxin efflux carriers at the plasma membrane (PM). Specifically, increase in H2O2 levels affects PIN2 endocytic recycling. We show that the PIN2 intracellular trafficking during adaptation to oxidative stress requires the function of the ADP-ribosylation factor (ARF)-guanine-nucleotide exchange factor (GEF) BEN1, an actin-associated regulator of the trafficking from the PM to early endosomes and, presumably, indirectly, trafficking to the vacuoles. We propose that H2O2 levels affect the actin dynamics thus modulating ARF-GEF-dependent trafficking of PIN2. This mechanism provides a way how root growth acclimates to stress and adapts to a changing environment.},
  author       = {Zwiewka, Marta and Bielach, Agnieszka and Tamizhselvan, Prashanth and Madhavan, Sharmila and Ryad, Eman Elrefaay and Tan, Shutang and Hrtyan, Mónika and Dobrev, Petre and Vanková, Radomira and Friml, Jiří and Tognetti, Vanesa B.},
  issn         = {1471-9053},
  journal      = {Plant and Cell Physiology},
  number       = {2},
  pages        = {255--273},
  publisher    = {Oxford University Press},
  title        = {{Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking}},
  doi          = {10.1093/pcp/pcz001},
  volume       = {60},
  year         = {2019},
}

@article{12196,
  abstract     = {SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in the induction of defense responses. However, the molecular mechanisms underlying NLR activation and the subsequent provocation of immune responses are only partially characterized. To identify negative regulators of NLR-mediated immunity, a forward genetic screen was undertaken to search for enhancers of the dwarf, autoimmune gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism, the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display wild-type-like morphology and resistance. M2 progeny were screened for mutant, snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes. The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated expression of the pPR2-GUS defense marker reporter gene and enhanced resistance to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning and Illumina sequencing, it was determined that the muse9 mutation is in the gene encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10. The syd-10 single mutant has no observable alteration from wild-type-like resistance, although the syd-4 T-DNA insertion allele displays enhanced resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated immunity. SYD may work with other proteins at the chromatin level to repress SNC1 transcription; such regulation is important for fine-tuning the expression of NLR-encoding genes to prevent unpropitious autoimmunity.},
  author       = {Johnson, Kaeli C.M. and Xia, Shitou and Feng, Xiaoqi and Li, Xin},
  issn         = {0032-0781},
  journal      = {Plant and Cell Physiology},
  keywords     = {Cell Biology, Plant Science, Physiology, General Medicine},
  number       = {8},
  pages        = {1616--1623},
  publisher    = {Oxford University Press},
  title        = {{The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity}},
  doi          = {10.1093/pcp/pcv087},
  volume       = {56},
  year         = {2015},
}