AT-hook transcription factors repress petiole growth by antagonizing PIF4
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ABSTRACT:
PROVIDER: PRJNA505274 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8181350.fastq.gz | Fastqsanger.gz | |||
| SRR8181351.fastq.gz | Fastqsanger.gz | |||
| SRR8181342.fastq.gz | Fastqsanger.gz | |||
| SRR8181352.fastq.gz | Fastqsanger.gz | |||
| SRR8181343.fastq.gz | Fastqsanger.gz |
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Project description:As sessile organisms, plants rely heavily on growth and developmental plasticity to respond to external challenges threatening their survival. Strict regulation of growth in organs such as hypocotyls and petioles enables plants to respond optimally to varying environmental conditions, such as changes in light and temperature, while also ensuring that resources are not needlessly wasted on unnecessary growth. Studies performed in Arabidopsis thaliana have established the PHYTOCHROME INTERACTING FACTOR (PIF) transcription factor family as key positive regulators of growth, particularly in hypocotyls and petioles. In this study, we identify members of the AT-HOOK MOTIF NUCLEAR LOCALIZED (AHL) family, including SUPPRESSOR OF PHYTOCHROME B4-#3 (SOB3), as repressors of PIF4-mediated petiole elongation. Specifically, we found that high levels of SOB3 lead to a short-petiole phenotype similar to that conferred by removal of PIF4. Conversely, the dominant-negative sob3-6 mutant has long petioles, a phenotype which is dependent on PIF4. Additionally, we show that AHLs repress the expression of many PIF-activated genes, including a number involved in hormone-mediated promotion of growth and a subset of which are directly bound by both SOB3 and PIFs. Taken together these results suggest that AHLs repress petiole growth by antagonizing PIF-mediated transcriptional activation of growth-promoting genes, including ARABIDOPSIS THALIANA HOMEOBOX PROTEIN 2 (ATHB2), BRASSINOSTEROID INSENSITIVE 1 (BRI1), INDOLE-3-ACETIC ACID INDUCIBLE 19 (IAA19), PIN-FORMED 3 (PIN3), SMALL AUXIN UP RNA 24 (SAUR24), and YUCCA8 (YUC8). Elucidating a mechanism by which positive and negative growth factors influence growth in petioles achieves a critical first step towards understanding the gene regulatory networks which modulate leaf growth in response to the environment.
2020-03-19 | GSE122455 | GEO
Project description:As sessile organisms, plants rely heavily on growth and developmental plasticity to respond to external challenges threatening their survival. Strict regulation of growth in organs such as hypocotyls and petioles enables plants to respond optimally to varying environmental conditions, such as changes in light and temperature, while also ensuring that resources are not needlessly wasted on unnecessary growth. Studies performed in Arabidopsis thaliana have established the PHYTOCHROME INTERACTING FACTOR (PIF) transcription factor family as key positive regulators of growth, particularly in hypocotyls and petioles. In this study, we identify members of the AT-HOOK MOTIF NUCLEAR LOCALIZED (AHL) family, including SUPPRESSOR OF PHYTOCHROME B4-#3 (SOB3), as repressors of PIF4-mediated petiole elongation. Specifically, we found that high levels of SOB3 lead to a short-petiole phenotype similar to that conferred by removal of PIF4. Conversely, the dominant-negative sob3-6 mutant has long petioles, a phenotype which is dependent on PIF4. Additionally, we show that AHLs repress the expression of many PIF-activated genes, including a number involved in hormone-mediated promotion of growth and a subset of which are directly bound by both SOB3 and PIFs. Taken together these results suggest that AHLs repress petiole growth by antagonizing PIF-mediated transcriptional activation of growth-promoting genes, including ARABIDOPSIS THALIANA HOMEOBOX PROTEIN 2 (ATHB2), BRASSINOSTEROID INSENSITIVE 1 (BRI1), INDOLE-3-ACETIC ACID INDUCIBLE 19 (IAA19), PIN-FORMED 3 (PIN3), SMALL AUXIN UP RNA 24 (SAUR24), and YUCCA8 (YUC8). Elucidating a mechanism by which positive and negative growth factors influence growth in petioles achieves a critical first step towards understanding the gene regulatory networks which modulate leaf growth in response to the environment.
2020-03-19 | GSE122454 | GEO
Project description:AT-hook transcription factors repress petiole growth by antagonizing PIF4 [RNA-seq]
| PRJNA505275 | ENA
Project description:AT-hook transcription factors repress petiole growth by antagonizing PIF4 [ChIP-seq]
| PRJNA505276 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-03-19 | GSE122456 | GEO
Project description:Light signaling precisely controls the photomorphogenic development in plants. In this study, we report COP1 SUPPRESSOR 6 (CSU6) function as positive regulator of light signaling. Loss of CSU6 function largely rescued the cop1-6 constitutively photomorphogenic phenotype. The hypocotyl length of csu6 mutant seedlings was shorter in the dark, but longer than that of wide-type in the light. CSU6 not only associated with the promoter regions of PIF4 and PIF5 to inhibit their expression during the day, but also directly interacts with both PIF4 and PIF5 to repress their transcriptional activity. CSU6 negatively controls a large group of PIF4- and PIF5-mediated genes' expression. Mutations in PIF4 and/or PIF5 are epistatic to the loss of CSU6, suggesting that CSU6 acts upstream of PIF4 and PIF5. Taken together, CSU6 promotes photomorphogenesis by negatively regulating PIF4 and PIF5 transcription and biochemical activity.
2024-04-23 | GSE201389 | GEO
Project description:Light-induced phosphorylation is necessary and essential for the degradation of phytochrome-interacting factors (PIFs), the central repressors of photomorphogenesis. Although the kinases responsible for PIF phosphorylation have been extensively studied, the phosphatases underlying PIF dephosphorylation are largely unknown. Here, we real that mutation of FyPP1 and FyPP3, two catalytic subunits of PP6 phosphatases, promoted photomorphogenesis of seedlings in the dark. PP6 and PIFs functioned synergistically to repress photomorphogenesis. FyPP1 and FyPP3 directly interacted with and dephosphorylated PIF3 and PIF4. The light-induced degradation of PIF4 and the PIF transcriptional activities were dependent on PP6 activity. These data demonstrate that PP6 phosphatases repress photomorphogenesis through regulation of PIF phosphorylation, protein stability and transcriptional activity.
2019-09-04 | GSE128498 | GEO
Project description:To investigate the effect of the interaction between the MRG1/2 and PIF4, here we analysed differentially expressed genes compared to the mutant and wild-type by RNA-seq under different temperature. We performed gene expression profiling analysis using data obtained from RNA-seq of WT, mrg1 mrg2, pif4, and mrg1 mrg2 pif4 plants at 22degC and 28degC.
2024-01-04 | GSE213025 | GEO
Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF4, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF4 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF4-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF4 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.
2014-10-02 | E-GEOD-43284 | biostudies-arrayexpress
Project description:In plants, an elevation in ambient temperature induces morphological changes including elongation hypocotyls, considered to be adaptive responses to alleviate the heat-induced damages. The high temperature-induced morphological changes are called thermomorphogenesis, which is predominantly regulated by a bHLH transcription factor PIF4. Although PIF4 is expressed in all aerial tissues including the epidermis, mesophyll, and vascular bundle, its tissue-specific functions in thermomorphogenesis are not known. Here, we found that epidermis-specific expression of PIF4 induced constitutive long hypocotyls, while vasculature-specific expression of PIF4 had no effect on hypocotyl growth. Consistently, RNA-Seq and qRT-PCR analyses revealed that auxin responsive genes and growth-related genes were highly activated by epidermal, but not by vascular, PIF4. The epidermal, but not vascular, inactivation of PIF4 by a PIF4 artificial microRNA or a dominant negative form of PIF4 suppressed thermoresponsive gene expression and hypocotyl growth. Additionally, both the block of epidermal auxin signaling and the epidermal overexpression of a thermosensor phytochrome B (phyB) inhibited thermoresponsive growth, indicating that epidermal PIF4-auxin pathway are essential for the temperature responses. We further show that epidermal PIF4 is increased by high temperatures mainly through the transcriptional activation of PIF4. Taken together, our study demonstrates that the epidermis regulates thermoresponsive growth through the phyB-PIF4-auxin pathway.
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