Overexpression of BBX18 Promotes Thermomorphogenesis Through the PRR5-PIF4 Pathway.
Ontology highlight
ABSTRACT:
SUBMITTER: Hwang G
PROVIDER: S-EPMC8651621 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Plants respond to high ambient temperature by implementing a suite of morphological changes collectively termed thermomorphogenesis. Here we show that the above and below ground tissue-response to high ambient temperature are mediated by distinct transcription factors. While the central hub transcription factor, PHYTOCHROME INTERCTING FACTOR 4 (PIF4) regulates the above ground tissue response, the below ground root elongation is primarily regulated by ELONGATED HYPOCOTYL 5 (HY5). Plants respond to high temperature by largely expressing distinct sets of genes in a tissue-specific manner. HY5 promotes root thermomorphogenesis via directly controlling the expression of many genes including the auxin and BR pathway genes. Strikingly, the above and below ground thermomorphogenesis is impaired in spaQ. Because SPA1 directly phosphorylates PIF4 and HY5, SPAs might control the stability of PIF4 and HY5 to regulate thermomorphogenesis in both tissues. These data collectively suggest that plants employ distinct combination of SPA-PIF4-HY5 module to regulate tissue-specific thermomorphogenesis.
| S-EPMC8209091 | biostudies-literature
Project description:Plants display thermomorphogenesis in response to high temperature (HT). PHYTOCHROME INTERACTING FACTOR 4 (PIF4) is a central integrator regulated by numerous negative regulators. However, the mechanisms underpinning PIF4 positive regulation are largely unknown. Here, we find that TEOSINTE BRANCHED 1/CYCLOIDEA/PCF 5 (TCP5), TCP13, and TCP17 transcription factors promote the activity of PIF4 at transcriptional and post-transcriptional levels. TCP5 is rapidly induced by HT treatment, and TCP5 protein stability increases under HT. The overexpression of TCP5 causes constitutive thermomorphogenic phenotypes, whereas the tcp5 tcp13 tcp17 triple mutant exhibits aberrant thermomorphogenesis. We demonstrate that TCP5 not only physically interacts with PIF4 to enhance its activity but also directly binds to the promoter of PIF4 to increase its transcript. TCP5 and PIF4 share common downstream targets. The tcp5 tcp13 tcp17 mutant partially restores the long hypocotyls caused by PIF4 overexpression. Our findings provide a layer of understanding about the fine-scale regulation of PIF4 and plant thermomorphogenesis.
| S-EPMC6548983 | biostudies-literature
Project description:Daytime warm temperature elicits thermomorphogenesis in Arabidopsis by stabilizing the central thermoregulator PHYTOCHROME INTERACTING transcription FACTOR 4 (PIF4), whose degradation is otherwise promoted by the photoreceptor and thermosensor phytochrome B. PIF4 stabilization in the light requires a transcriptional activator, HEMERA (HMR), and is abrogated when HMR's transactivation activity is impaired in hmr-22. Here, we report the identification of a hmr-22 suppressor mutant, rcb-101, which surprisingly carries an A275V mutation in REGULATOR OF CHLOROPLAST BIOGENESIS (RCB). rcb-101/hmr-22 restores thermoresponsive PIF4 accumulation and reverts the defects of hmr-22 in chloroplast biogenesis and photomorphogenesis. Strikingly, similar to hmr, the null rcb-10 mutant impedes PIF4 accumulation and thereby loses the warm-temperature response. rcb-101 rescues hmr-22 in an allele-specific manner. Consistently, RCB interacts directly with HMR. Together, these results unveil RCB as a novel temperature signaling component that functions collaboratively with HMR to initiate thermomorphogenesis by selectively stabilizing PIF4 in the daytime.
| S-EPMC8024306 | biostudies-literature
Project description:High temperature activates the transcription factor PHYTOCHROME-INTERACTING FACTOR4 (PIF4) to stimulate auxin signaling, which causes hypocotyl elongation and leaf hyponasty (thermomorphogenesis). HOOKLESS1 (HLS1) is a recently reported positive regulator of thermomorphogenesis, but the molecular mechanisms by which HLS1 regulates thermomorphogenesis remain unknown. In this study, we initially compared PIF4- and/or HLS1-dependent differential gene expression (DEG) upon high-temperature treatment. We found that a large number of genes are coregulated by PIF4 and HLS1, especially genes involved in plant growth or defense responses. Moreover, we found that HLS1 interacts with PIF4 to form a regulatory module and that, among the HLS1-PIF4-coregulated genes, 27.7% are direct targets of PIF4. We also identified 870 differentially alternatively spliced genes (DASGs) in wild-type plants under high temperature. Interestingly, more than half of these DASG events (52.4%) are dependent on both HLS1 and PIF4, and the spliceosome-defective mutant plantsexhibit a hyposensitive response to high temperature, indicating that DASGs are required for thermomorphogenesis. Further comparative analyses showed that the HLS1/PIF4-coregulated DEGs and DASGs exhibit almost no overlap, suggesting that high temperature triggers two distinct strategies to control plant responses and thermomorphogenesis. Taken together, these results demonstrate that the HLS1-PIF4 module precisely controls both transcriptional and posttranscriptional regulation during plant thermomorphogenesis.
| S-EPMC7748007 | biostudies-literature
Project description:High ambient temperature attributable to global warming has a profound influence on plant growth and development at all stages of the life cycle. The response of plants to high ambient temperature, termed thermomorphogenesis, is characterized by hypocotyl and petiole elongation and hyponastic growth at the seedling stage. However, our understanding of the molecular mechanism of thermomorphogenesis is still rudimentary. Here, we show that a set of four SUPPRESSOR OF PHYA-105 (SPA) genes is required for thermomorphogenesis. Consistently, SPAs are necessary for global changes in gene expression in response to high ambient temperature. In the spaQ mutant at high ambient temperature, the level of SPA1 is unaffected, whereas the thermosensor phytochrome B (phyB) is stabilized. Furthermore, in the absence of four SPA genes, the pivotal transcription factor PIF4 fails to accumulate, indicating a role of SPAs in regulating the phyB-PIF4 module at high ambient temperature. SPA1 directly phosphorylates PIF4 in vitro, and a mutant SPA1 affecting the kinase activity fails to rescue the PIF4 level in addition to the thermo-insensitive phenotype of spaQ, suggesting that the SPA1 kinase activity is necessary for thermomorphogenesis. Taken together, these data suggest that SPAs are new components that integrate light and temperature signaling by fine-tuning the phyB-PIF4 module.
| S-EPMC7561471 | biostudies-literature
Project description:In plants, an elevation in ambient temperature induces adaptive morphological changes including elongated hypocotyls, 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 show that epidermis-specific expression of PIF4 induces constitutive long hypocotyls, while vasculature-specific expression of PIF4 has no effect on hypocotyl growth. RNA-Seq and qRT-PCR analyses reveal that auxin-responsive genes and growth-related genes are highly activated by epidermal, but not by vascular, PIF4. Additionally, inactivation of epidermal PIF4 or auxin signaling, and overexpression of epidermal phyB suppresses thermoresponsive growth, indicating that epidermal PIF4-auxin pathways are essential for the temperature responses. Further, we show that high temperatures increase both epidermal PIF4 transcription and the epidermal PIF4 DNA-binding ability. Taken together, our study demonstrates that the epidermis regulates thermoresponsive growth through the phyB-PIF4-auxin pathway.
| S-EPMC7044213 | biostudies-literature
Project description:Krüppel-like factor 4 (KLF4) is a transcription factor and functions as a tumor suppressor or tumor promoter in different cancer types. KLF4 regulates many gene expression, thus affects the process of cell proliferation, differentiation, and apoptosis. Recently, KLF4 was reported to induce senescence during the generation of induced pluripotent stem (iPS) cells, but the exact mechanism is still unclear. In this study, we constructed two doxycycline-inducing KLF4 cell models, and demonstrated overexpression of KLF4 could promote cell senescence, detected by senescence-associated ?-galactosidase activity assay. Then we confirmed that p21, a key effector of senescence, was directly induced by KLF4. KLF4 could also inhibit survivin, which could indirectly induce p21. By miRNA microarray, we found a series of miRNAs regulated by KLF4 and involved in senescence. We demonstrated that KLF4 could upregulate miR-203, and miR-203 contributed to senescence through miR-203-survivin-p21 pathway. Our results suggest that KLF4 could promote cell senescence through a complex network: miR-203, survivin, and p21, which were all regulated by overexpression of KLF4 and contributed to cell senescence.
| S-EPMC5312384 | biostudies-literature
Project description:N-myc down-regulated gene 1 (NDRG1) has been shown to regulate tumor growth and metastasis in various malignant tumors and also to be dysregulated in esophageal squamous cell carcinoma (ESCC). Here, we show that NDRG1 overexpression (91.9%, 79/86) in ESCC tumor tissues is associated with poor overall survival of esophageal cancer patients. When placed in stable transfectants of the KYSE 30 ESCC cell line generated by lentiviral transduction with the ectopic overexpression of NDRG1, the expression of transducin-like enhancer of Split 2 (TLE2) was decreased sharply, however ?-catenin was increased. Mechanistically, NDRG1 physically associates with TLE2 and ?-catenin to affect the Wnt pathway. RNA interference and TLE2 overexpression studies demonstrate that NDRG1 fails to active Wnt pathway compared with isogenic wild-type controls. Strikingly, NDRG1 overexpression induces the epithelial mesenchymal transition (EMT) through activating the Wnt signaling pathway in ESCC cells, decreased the expression of E-cadherin and enhanced the expression of Snail. Our study elucidates a mechanism of NDRG1-regulated Wnt pathway activation and EMT via affecting TLE2 and ?-catenin expression in esophageal cancer cells. This indicates a pro-oncogenic role for NDRG1 in esophageal cancer cells whereby it modulates tumor progression.
| S-EPMC5036407 | biostudies-literature
Project description:Osteosarcoma (OS) is a kind of malignant bone tumor that occurs frequently in the region surrounding the knee joint and poses a threat to the health of teenagers. Since the application of chemotherapy to treat OS, 5-year survival rate in patients has improved from 10% to 70%, but patient survival has not changed over the past four decades. Coactivator-associated arginine methyltransferase 1 (CARM1) is a member of the PRMT protein family; it acts as an oncogene in many cancers, but its function in OS is still unknown. In this study, we found that CARM1 is overexpressed in OS and its expression is correlated with the Enneking stage. CCK-8 and colony forming assays showed that proliferation in OS cell lines was downregulated when siRNA was used to knockdown CARM1 expression. The cell cycle was inhibited in S phase after si-CARM1 transfection in OS cell lines. An antibody array indicated that Erk1/2 (Thr202/Tyr204), PARS40 (Thr246), and GSK3? (Ser9) expression are affected by CARM1, and western blotting verified that CARM1 promotes OS cell proliferation via pGSK3?/?-catenin/cyclinD1 signaling. Accordingly, CARM1 is a crucial gene in OS and is a potential new treatment target.
| S-EPMC5599903 | biostudies-other
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.
2020-01-26 | GSE133564 | GEO