Flowering of Arabidopsis is regulated by several environmental and endogenous signals. An important integrator of these inputs is the FLOWERING LOCUS T (FT) gene, which encodes a small, possibly mobile protein. A primary response to floral induction is the activation of FT RNA expression in leaves. Because flowers form at a distant site, the shoot apex, these data suggest that FT primarily controls the timing of flowering. Integration of temporal and spatial information is mediated in part by the bZIP transcription factor FD, which is already expressed at the shoot apex before floral induction. A complex of FT and FD proteins in turn can activate floral identity genes such as APETALA1 (AP1).
The balance between cellular proliferation and differentiation is a key aspect of development in multicellular organisms. Using high-resolution expression data from the Arabidopsis root, we identified a transcription factor, UPBEAT1 (UPB1), that regulates this balance. Genomewide expression profiling coupled with ChIP-chip analysis revealed that UPB1 directly regulates the expression of a set of peroxidases that modulate the balance of reactive oxygen species (ROS) between the zones of cell proliferation and the zone of cell elongation where differentiation begins. Disruption of UPB1 activity alters this ROS balance, leading to a delay in the onset of differentiation. Modulation of either ROS balance or peroxidase activity through chemical reagents affects the onset of differentiation in a manner consistent with the postulated UPB1 function. This pathway functions independently of auxin and cytokinin plant hormonal signaling. Comparison to ROS-regulated growth control in animals suggests that a similar mechanism is used in plants and animals.
Global population increases and climate change underscore the need for better comprehension of how plants acquire and process nutrients such as iron. Using cell type-specific transcriptional profiling, we identified a pericycle-specific iron deficiency response and a bHLH transcription factor, POPEYE (PYE), that may play an important role in this response. Functional analysis of PYE suggests that it positively regulates growth and development under iron-deficient conditions. Chromatin immunoprecipitation-on-chip analysis and transcriptional profiling reveal that PYE helps maintain iron homeostasis by regulating the expression of known iron homeostasis genes and other genes involved in transcription, development, and stress response. PYE interacts with PYE homologs, including IAA-Leu Resistant3 (ILR3), another bHLH transcription factor that is involved in metal ion homeostasis. Moreover, ILR3 interacts with a third protein, BRUTUS (BTS), a putative E3 ligase protein, with metal ion binding and DNA binding domains, which negatively regulates the response to iron deficiency. PYE and BTS expression is also tightly coregulated. We propose that interactions among PYE, PYE homologs, and BTS are important for maintaining iron homeostasis under low iron conditions.
Plants continuously maintain pools of totipotent stem cells in their apical meristems from which elaborate root and shoot systems are produced. In Arabidopsis thaliana, stem cell fate in the shoot apical meristem is controlled by a regulatory network that includes the CLAVATA (CLV) ligand-receptor system and the homeodomain protein WUSCHEL (WUS). Phytohormones such as auxin and cytokinin are also important for meristem regulation. Here we show a mechanistic link between the CLV/WUS network and hormonal control. WUS, a positive regulator of stem cells, directly represses the transcription of several two-component ARABIDOPSIS RESPONSE REGULATOR genes (ARR5, ARR6, ARR7 and ARR15), which act in the negative-feedback loop of cytokinin signalling. These data indicate that ARR genes might negatively influence meristem size and that their repression by WUS might be necessary for proper meristem function. Consistent with this hypothesis is our observation that a mutant ARR7 allele, which mimics the active, phosphorylated form, causes the formation of aberrant shoot apical meristems. Conversely, a loss-of-function mutation in a maize ARR homologue was recently shown to cause enlarged meristems.
The development of multicellular organisms relies on the coordinated control of cell divisions leading to proper patterning and growth [1][2][3] . The molecular mechanisms underlying pattern formation, particularly the regulation of formative cell divisions, remain poorly understood. In Arabidopsis, formative divisions generating the root ground tissue are controlled by SHORTROOT (SHR) and SCARECROW (SCR) 4-6. Here we show, using cell-type-specific transcriptional effects of SHR and SCR combined with data from chromatin immunoprecipitation-based microarray experiments, that SHR regulates the spatiotemporal activation of specific genes involved in cell division. Coincident with the onset of a specific formative division, SHR and SCR directly activate a D-type cyclin; furthermore, altering the expression of this cyclin resulted in formative division defects. Our results indicate that proper pattern formation is achieved through transcriptional regulation of specific cellcycle genes in a cell-type-and developmental-stage-specific context. Taken together, we provide evidence for a direct link between developmental regulators, specific components of the cell-cycle machinery and organ patterning.Growth and patterning are key processes that govern the development of multicellular organisms. In some cases, like early Drosophila embryogenesis 7 , these are independent. However, in many animals and plants, proper development frequently relies on tight coordination of growth and patterning. Disruption of this coordination can lead to unchecked cell growth, resulting in tumorigenesis or misshapen organs 8 . Although the molecular mechanisms involved in pattern formation 9-11 and in cell-cycle control [12][13][14][15] 5,6,23,24,25 . To gain insight into the role of the SHR/SCR network in controlling formative cell divisions, we expressed an inducible version of either SHR or SCR in its respective mutant background and characterized the timing of formative divisions after induction.Before induction, SHR-and SCR-inducible plants had a single mutant ground tissue layer 4,5 (Supplementary Fig. 1). After SHR induction, SCR expression was observed within 3 h, indicating that SHR rapidly activates its targets ( Supplementary Fig. 1). The first periclinal (parallel to the direction of growth) division in the mutant ground tissue layer occurred 6 h after SHR induction (Fig. 1a , Supplementary Fig. 1 and Supplementary Movie 1) and earlier after SCR induction (Fig. 1b). Two layers of ground tissue with SCR expression in the quiescent centre and endodermis (Supplementary Fig. 1), along with a nearly complete Casparian band 5 , were detected 24 h after SHR induction ( Supplementary Fig. 2). This underlines the combinatorial role of SHR and SCR in regulating formative cell divisions and also indicates that the two inducible systems have slightly different kinetics.To understand the dynamics of the SHR/SCR regulatory network, we sorted ground tissue cells at several time points after SHR and SCR induction and performed microarray a...
The processing of Arabidopsis thaliana microRNAs (miRNAs) from longer primary transcripts (pri-miRNAs) requires the activity of several proteins, including DICER-LIKE1 (DCL1), the double-stranded RNA-binding protein HYPONASTIC LEAVES1 (HYL1), and the zinc finger protein SERRATE (SE). It has been noted before that the morphological appearance of weak se mutants is reminiscent of plants with mutations in ABH1/CBP80 and CBP20, which encode the two subunits of the nuclear cap-binding complex. We report that, like SE, the cap-binding complex is necessary for proper processing of pri-miRNAs. Inactivation of either ABH1/CBP80 or CBP20 results in decreased levels of mature miRNAs accompanied by apparent stabilization of pri-miRNAs. Whole-genome tiling array analyses reveal that se, abh1/cbp80, and cbp20 mutants also share similar splicing defects, leading to the accumulation of many partially spliced transcripts. This is unlikely to be an indirect consequence of improper miRNA processing or other mRNA turnover pathways, because introns retained in se, abh1/cbp80, and cbp20 mutants are not affected by mutations in other genes required for miRNA processing or for nonsense-mediated mRNA decay. Taken together, our results uncover dual roles in splicing and miRNA processing that distinguish SE and the cap-binding complex from specialized miRNA processing factors such as DCL1 and HYL1. P osttranscriptional gene regulation by microRNAs (miRNAs) is essential for the development and function of multicellular eukaryotes (1). In plants, miRNAs are processed from primary transcripts that contain partially complementary foldbacks of variable lengths (pri-miRNAs). Pri-miRNAs are similar to messenger RNAs (mRNAs) in being transcribed by DNA-dependent RNA polymerase II (pol II) and carrying a seven-methyl guanosine (m 7 G) cap at the 5Ј end and a polyadenosine (polyA) tail at the 3Ј end (1). Pri-miRNAs are processed to yield 20-to 22-nt-long mature miRNAs by an RNAseIII-like domain containing protein called DICER-LIKE1 (DCL1) (2-4). DCL1 interacts with the double-stranded (ds)RNA-binding protein HYPONASTIC LEAVES1 (HYL1) and the zinc finger protein SERRATE (SE) to ensure proper processing of pri-miRNAs (5-13). In common with dcl1 mutants, pri-miRNA levels are increased in plants that lack HYL1 or SE activity, whereas the amounts of mature miRNAs are reduced (5-9). All three proteins are found in nuclear processing centers, called D-bodies or SmD3/SmB nuclear bodies (12, 13).Mutants deficient in miRNA biogenesis suffer from a large range of morphological defects. Plants with null alleles of DCL1 or SE die as embryos, and even moderate reduction of DCL1 activity leads to a broad spectrum of developmental abnormalities (8,14,15). The weak se-1 allele causes only mild defects, including an alteration of phyllotaxis and the name-sake serrated leaves (16,17). It has been noted before that the se-1 phenotype is reminiscent of that of another mutant with impaired RNA metabolism, ABA hypersensitive 1 (abh1). Both mutants respond more strongly t...
SummaryIn order to assess specific functional roles of plant heat shock transcription factors (HSF) we conducted a transcriptome analysis of Arabidopsis thaliana hsfA1a/hsfA1b double knock out mutants and wild-type plants. We used Affymetrix ATH1 microarrays (representing more than 24 000 genes) and conducted hybridizations for heat-treated or non-heat-treated leaf material of the respective lines. Heat stress had a severe impact on the transcriptome of mutant and wild-type plants. Approximately 11% of all monitored genes of the wild type showed a significant effect upon heat stress treatment. The difference in heat stress-induced gene expression between mutant and wild type revealed a number of HsfA1a/1b-regulated genes. Besides several heat shock protein and other stress-related genes, we found HSFA-1a/1b-regulated genes for other functions including protein biosynthesis and processing, signalling, metabolism and transport. By screening the profiling data for genes in biochemical pathways in which known HSF targets were involved, we discovered that at each step in the pathway leading to osmolytes, the expression of genes is regulated by heat stress and in several cases by HSF. Our results document that in the immediate early phase of the heat shock response HSF-dependent gene expression is not limited to known stress genes, which are involved in protection from proteotoxic effects. HsfA1a and HsfA1b-regulated gene expression also affects other pathways and mechanisms dealing with a broader range of physiological adaptations to stress.
Stem cell function during organogenesis is a key issue in developmental biology. The transcription factor SHORT-ROOT (SHR) is a critical component in a developmental pathway regulating both the specification of the root stem cell niche and the differentiation potential of a subset of stem cells in the Arabidopsis root. To obtain a comprehensive view of the SHR pathway, we used a statistical method called meta-analysis to combine the results of several microarray experiments measuring the changes in global expression profiles after modulating SHR activity. Meta-analysis was first used to identify the direct targets of SHR by combining results from an inducible form of SHR driven by its endogenous promoter, ectopic expression, followed by cell sorting and comparisons of mutant to wild-type roots. Eight putative direct targets of SHR were identified, all with expression patterns encompassing subsets of the native SHR expression domain. Further evidence for direct regulation by SHR came from binding of SHR in vivo to the promoter regions of four of the eight putative targets. A new role for SHR in the vascular cylinder was predicted from the expression pattern of several direct targets and confirmed with independent markers. The meta-analysis approach was then used to perform a global survey of the SHR indirect targets. Our analysis suggests that the SHR pathway regulates root development not only through a large transcription regulatory network but also through hormonal pathways and signaling pathways using receptor-like kinases. Taken together, our results not only identify the first nodes in the SHR pathway and a new function for SHR in the development of the vascular tissue but also reveal the global architecture of this developmental pathway.
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