Auxin Induced Endodermal to QC Transdifferentiation Time Series and Downsteam of JKD Analysis
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ABSTRACT: First series collects endodermal cells using the SCR::GFP promoter after treatment with auxin Second series includes comparative samples of jkd vs. wild type plants for specific tissues; QC and meristem
Project description:First series collects endodermal cells using the SCR::GFP promoter after treatment with auxin Second series includes comparative samples of jkd vs. wild type plants for specific tissues; QC and meristem In first series, plants are grown under normal conditions, then transferred to auxin analog 2,4-D and endodermis is collected at time points 0hrs, 24hrs, 48hrs, 72hrs, 96 hrs.
Project description:We report the discovery of a root growth program in Arabidopsis that is independent of a functional quiescent center (QC). In this regulatory program, PHABULOSA (PHB), posttranscriptionally regulated by SHR and SCR, plays a central role. In phb shr and phb scr mutants, root meristem/growth activity recovers significantly. Interestingly, this recovery does not accompany the resurgence of QC cells. PHB regulates apical root growth in stele cells of the root meristem, located proximal to the QC. Our genome-wide investigation suggests that PHB exerts its influence on root growth by regulating auxin-cytokinin homeostasis. Apical root growth was restored when cytokinin levels were genetically reduced in the shr mutant. Conversely, when miRNA-resistant PHB was expressed in the root stele cells, apical root growth and meristem functions were significantly inhibited without blocking the QC identity. Taken together, our investigation reveals two mechanisms through which SHR regulates root growth and stem cell activities: one is to specify and maintain the QC and the other is to regulate the proximal meristem activity through PHB and cytokinin. In this regulation, QC seems to be more involved in maintaining the “growth signal” and thus ensure the indeterminate root growth.
Project description:Transcriptional profiling of dark-grown Arabidopsis seedlings comparing SCR:PIF1/pifQ transgenic plant with pif1pif3pif4pif5 quadruple mutant (pifQ). Seedlings were grown under dark condition for 2.5 days. Goal was to determine the effects of endodermal PIF1 in dark-grown seedlings. Two-condition experiment, SCR:PIF1/pifQ vs. pifQ Biological replicates: 3 pifQ replicates, 3 SCR:PIF1 replicates.
Project description:Here we show that differntiated endodermal cells have a distinct transcriptional response to auxin treatment. We perform a time serie of 10µM NAA treatment and sample at t=0, 2, 4, 8, 16 and 24hrs after NAA treatment. For the time series we compared roots of the solitairy root 1 (slr-1) mutant to the CASP1::shy2-2/slr-1 double mutant. We also provide RNAseq data of slr-1, CASP1::shy2-2 and CASP1::shy2-2/slr-1 at t=0
Project description:The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells.
Project description:We report the discovery of a root growth program in Arabidopsis that is independent of a functional quiescent center (QC). In this regulatory program, PHABULOSA (PHB), posttranscriptionally regulated by SHR and SCR, plays a central role. In phb shr and phb scr mutants, root meristem/growth activity recovers significantly. Interestingly, this recovery does not accompany the resurgence of QC cells. PHB regulates apical root growth in stele cells of the root meristem, located proximal to the QC. Our genome-wide investigation suggests that PHB exerts its influence on root growth by regulating auxin-cytokinin homeostasis. Apical root growth was restored when cytokinin levels were genetically reduced in the shr mutant. Conversely, when miRNA-resistant PHB was expressed in the root stele cells, apical root growth and meristem functions were significantly inhibited without blocking the QC identity. Taken together, our investigation reveals two mechanisms through which SHR regulates root growth and stem cell activities: one is to specify and maintain the QC and the other is to regulate the proximal meristem activity through PHB and cytokinin. In this regulation, QC seems to be more involved in maintaining the M-bM-^@M-^\growth signalM-bM-^@M-^] and thus ensure the indeterminate root growth. Total 7 samples (2 replicates of shr-2 mutant (high PHABULOSA expression) vs. 2 replicates of shr-2 phb-6 (low/absent PHABULOSA expression). 3 replicates of Wild type used as reference sample.
Project description:Transcriptional profiling of dark-grown Arabidopsis seedlings comparing SCR:PIF1/pifQ transgenic plant with pif1pif3pif4pif5 quadruple mutant (pifQ). Seedlings were grown under dark condition for 2.5 days. Goal was to determine the effects of endodermal PIF1 in dark-grown seedlings.
Project description:The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells. ChIP-seq analysis of genes bound by the ERF115 transcription factor, using mock ChIP with wild type cells as negative control. Analyzed by Illumina HiSeq
Project description:Glutaminyl cyclase (QC) activity in macrophage cells is correlated with the gene expression of MCP-2 and QC-catalyzed N-terminal pGlu formation of MCPs is required for macrophage migration and provide new insights into the role of QC in the inflammation process.