Similar Datasets
Project description:MicroRNAs (miRNAs) play diverse roles in plant development, but whether and how miRNAs participate in thermomorphogenesis remain ambiguous. Here we show that HYPONASTIC LEAVES 1 (HYL1)-a key component of miRNA biogenesis-acts downstream of the thermal regulator PHYTOCHROME INTERACTING FACTOR 4 in the temperature-dependent plasticity of hypocotyl growth in Arabidopsis. A hyl1-2 suppressor screen identified a dominant dicer-like1 allele that rescues hyl1-2's defects in miRNA biogenesis and thermoresponsive hypocotyl elongation. Genome-wide miRNA and transcriptome analysis revealed microRNA156 (miR156) and its target SQUAMOSA PROMOTER-BINDING-PROTEIN-LIKE 9 (SPL9) to be critical regulators of thermomorphogenesis. Surprisingly, perturbation of the miR156/SPL9 module disengages seedling responsiveness to warm temperatures by impeding auxin sensitivity. Moreover, miR156-dependent auxin sensitivity also operates in the shade avoidance response at lower temperatures. Thus, these results unveil the miR156/SPL9 module as a previously uncharacterized genetic circuit that enables plant growth plasticity in response to environmental temperature and light changes.
| S-EPMC10033679 | biostudies-literature
Project description:MicroRNAs (miRNAs) play diverse roles in plant development, but whether and how miRNAs participate in thermomorphogenesis remains ambiguous. Here we show that HYPONASTIC LEAVES1 (HYL1) – a key component of microRNA biogenesis – acts downstream of the thermal regulator PHYTOCHROME INTERACTING FACTOR 4 in temperature-dependent plasticity of hypocotyl growth in Arabidopsis. A hyl1-2 suppressor screen identified a dominant dicer-like1 (dcl1) allele, dcl1-24, which rescues hyl1-2’s defects in miRNA biosynthesis and warm temperature-induced hypocotyl elongation. Genome-wide miRNA and transcriptome analysis reveal microRNA156 (miR156) and its target SQUAMOSA PROMOTER-BINDING-LIKE 9 (SPL9) as critical regulators of thermomorphogenesis. Surprisingly, perturbation of the miR156/SPL9 module disengages seedling responsiveness to warm temperatures by impeding auxin sensitivity. Moreover, the miR156-dependent auxin sensitivity also operates in the shade avoidance response at lower temperatures. Thus, these results unveil the miRNA156/SPL9 module as a previously-uncharacterized genetic circuitry that enables plant growth plasticity in response to environmental temperature and light changes.
2023-02-11 | GSE216361 | GEO
Project description:MicroRNAs (miRNAs) play diverse roles in plant development, but whether and how miRNAs participate in thermomorphogenesis remains ambiguous. Here we show that HYPONASTIC LEAVES1 (HYL1) – a key component of microRNA biogenesis – acts downstream of the thermal regulator PHYTOCHROME INTERACTING FACTOR 4 in temperature-dependent plasticity of hypocotyl growth in Arabidopsis. A hyl1-2 suppressor screen identified a dominant dicer-like1 (dcl1) allele, dcl1-24, that rescues hyl1-2’s defects in miRNA biosynthesis and warm temperature-induced hypocotyl elongation. Genome-wide miRNA and transcriptome analysis reveal microRNA156 (miR156) and its target SQUAMOSA PROMOTER-BINDING-LIKE 9 (SPL9) as critical regulators of thermomorphogenesis. Surprisingly, perturbation of the miR156/SPL9 module disengages seedling responsiveness to warm temperatures by impeding auxin sensitivity. Moreover, the miR156-dependent auxin sensitivity also operates in the shade avoidance response at lower temperatures. Thus, these results unveil the miRNA156/SPL9 module as a previously-uncharacterized genetic circuitry that enables plant growth plasticity in response to environmental temperature and light changes.
2023-02-11 | GSE216360 | GEO
Project description:MicroRNA156 conditions auxin sensitivity to enable growth plasticity in response to environmental changes in Arabidopsis
| PRJNA893215 | ENA
Project description:MicroRNA156 conditions auxin sensitivity to enable growth plasticity in response to environmental changes in Arabidopsis (RNA-Seq)
| PRJNA893217 | ENA
Project description:MicroRNA156 conditions auxin sensitivity to enable growth plasticity in response to environmental changes in Arabidopsis (miRNA-Seq)
| PRJNA893218 | ENA
Project description:Root development is regulated by the tripeptide glutathione (GSH), a strong non-enzymatic antioxidant found in plants but with a poorly understood function in roots. Here, Arabidopsis mutants deficient in GSH biosynthesis (cad2, rax1, and rml1) and plants treated with the GSH biosynthesis inhibitor buthionine sulfoximine (BSO) showed root growth inhibition, significant alterations in the root apical meristem (RAM) structure (length and cell division), and defects in lateral root formation. Investigation of the molecular mechanisms of GSH action showed that GSH deficiency modulated total ubiquitination of proteins and inhibited the auxin-related, ubiquitination-dependent degradation of Aux/IAA proteins and the transcriptional activation of early auxin-responsive genes. However, the DR5 auxin transcriptional response differed in root apical meristem (RAM) and pericycle cells. The RAM DR5 signal was increased due to the up-regulation of the auxin biosynthesis TAA1 protein and down-regulation of PIN4 and PIN2, which can act as auxin sinks in the root tip. The transcription auxin response (the DR5 signal and expression of auxin responsive genes) in isolated roots, induced by a low (0.1 µM) auxin concentration, was blocked following GSH depletion of the roots by BSO treatment. A higher auxin concentration (0.5 µM) offset this GSH deficiency effect on DR5 expression, indicating that GSH deficiency does not completely block the transcriptional auxin response, but decreases its sensitivity. The ROS regulation of GSH, the active GSH role in cell proliferation, and GSH cross-talk with auxin assume a potential role for GSH in the modulation of root architecture under stress conditions.
| S-EPMC7697393 | biostudies-literature
Project description:Variable individual responses to environmental changes, such as phenotype plasticity, are heritable, with some genotypes being robust and others plastic. This variation for plasticity contributes to variance in complex traits as genotype-by-environment interactions (G × E). However, the genetic basis of this variability in responses to the same external stimuli is still largely unknown. In an earlier study of a large haploid segregant yeast population, genotype-by-genotype-by-environment interactions were found to make important contributions to the release of genetic variation in growth responses to alterations of the growth medium. Here, we explore the genetic basis for heritable variation of different measures of phenotype plasticity in the same dataset. We found that the central loci in the environmentally dependent epistatic networks were associated with overall measures of plasticity, while the specific measures of plasticity identified a more diverse set of loci. Based on this, a rapid one-dimensional genome-wide association (GWA) approach to overall plasticity is proposed as a strategy to efficiently identify key epistatic loci contributing to the phenotype plasticity. The study thus provided both analytical strategies and a deeper understanding of the complex genetic regulation of phenotype plasticity in yeast growth.
| S-EPMC7693874 | biostudies-literature
Project description:Asymmetric auxin distribution is instrumental for the differential growth that causes organ bending on tropic stimuli and curvatures during plant development. Local differences in auxin concentrations are achieved mainly by polarized cellular distribution of PIN auxin transporters, but whether other mechanisms involving auxin homeostasis are also relevant for the formation of auxin gradients is not clear. Here we show that auxin methylation is required for asymmetric auxin distribution across the hypocotyl, particularly during its response to gravity. We found that loss-of-function mutants in Arabidopsis IAA CARBOXYL METHYLTRANSFERASE1 (IAMT1) prematurely unfold the apical hook, and that their hypocotyls are impaired in gravitropic reorientation. This defect is linked to an auxin-dependent increase in PIN gene expression, leading to an increased polar auxin transport and lack of asymmetric distribution of PIN3 in the iamt1 mutant. Gravitropic reorientation in the iamt1 mutant could be restored with either endodermis-specific expression of IAMT1 or partial inhibition of polar auxin transport, which also results in normal PIN gene expression levels. We propose that IAA methylation is necessary in gravity-sensing cells to restrict polar auxin transport within the range of auxin levels that allow for differential responses.
| S-EPMC6042151 | biostudies-literature
Project description:Static magnetic field (SMF) plays important roles in biological processes of many living organisms. In plants, however, biological significance of SMF and molecular mechanisms underlying SMF action remain largely unknown. To address these questions, we treated Arabidopsis young seedlings with different SMF intensities and directions. Magnetic direction from the north to south pole was adjusted in parallel (N0) with, opposite (N180) and perpendicular to the gravity vector. We discovered that root growth is significantly inhanced by 600 mT treatments except for N180, but not by any 300 mT treatments. N0 treatments lead to more active cell division of the meristem, and higher auxin content that is regulated by coordinated expression of PIN3 and AUX1 in root tips. Consistently, N0-promoted root growth disappears in pin3 and aux1 mutants. Transcriptomic and gene ontology analyses revealed that in roots 85% of the total genes significantly down-regulated by N0 compared to untreatment are enriched in plastid biological processes, such as metabolism and chloroplast development. Lastly, no difference in root length is observed between N0-treated and untreated roots of the double cryptochrome mutant cry1 cry2. Taken together, our data suggest that SMF-regulated root growth is mediated by CRY and auxin signaling pathways in Arabidopsis.
| S-EPMC6779896 | biostudies-other