Similar Datasets
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
| PRJNA505274 | ENA
Project description:AT-hook transcription factors repress petiole growth by antagonizing PIF4 [ChIP-seq]
| PRJNA505276 | ENA
Project description:AT-hook transcription factors repress petiole growth by antagonizing PIF4 [RNA-seq]
| PRJNA505275 | ENA
Project description:Tgif1 (thymine-guanine-interacting factor 1) and Tgif2 repress gene expression by binding directly to DNA or interacting with transforming growth factor (TGF) β-responsive SMADs. Tgifs are essential for embryogenesis and may function in tumor progression. By analyzing both gain and loss of Tgif function in a well-established mouse model of intestinal cancer, we show that Tgifs promote adenoma growth in the context of mutant Apc (adenomatous polyposis coli). Despite the tumor-suppressive role of TGFβ signaling, transcriptome profiling of colon tumors suggests minimal effect of Tgifs on the TGFβ pathway. Instead, it appears that Tgifs, which are up-regulated in Apc mutant colon tumors, contribute to reprogramming metabolic gene expression. Integrating gene expression data from colon tumors with other gene expression and chromatin-binding data identifies a set of direct Tgif target genes encoding proteins involved in acetyl CoA and pyruvate metabolism. Analysis of both tumor and nontumor tissues indicates that these genes are targets of Tgif repression in multiple settings, suggesting that this is a core Tgif function. We propose that Tgifs play an important role in regulating basic energy metabolism in normal cells, and that this function of Tgifs is amplified in some cancers.
| S-EPMC6446543 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-03-23 | GSE180871 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-07-09 | GSE221660 | GEO
Project description:Inhibition of hypocotyl growth is a well-established UV-B-induced photomorphogenic response that is mediated by the UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8). However, the molecular mechanism by which UVR8 signaling triggers inhibition of hypocotyl growth is poorly understood. The bZIP protein ELONGATED HYPOCOTYL 5 (HY5) functions as the main positive regulatory transcription factor in the UVR8 signaling pathway, with HY5-HOMOLOG (HYH) playing a minor role. However, here we demonstrate that hy5 hyh double mutants maintain significant UVR8-dependent hypocotyl growth inhibition. We identify UVR8-dependent inhibition of the activities of bHLH transcription factors PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5 as part of the UVR8 signaling pathway, which results in inhibition of hypocotyl growth. The UVR8-mediated repression of several hypocotyl elongation-related genes is independent of HY5 and HYH but largely associated with UVR8-dependent degradation of PIF4 and PIF5, a process that consequently diminishes PIF4/5 target promoter occupancy. Taken together, our data indicate that UVR8-mediated inhibition of hypocotyl growth involves degradation of PIF4 and PIF5. These findings contribute to our mechanistic understanding of UVR8-induced photomorphogenesis and further support the function of PIFs as integrators of different photoreceptor signaling pathways.
| S-EPMC7027837 | biostudies-literature
Project description:Although the ovalbumin (Ov) gene has served as a model to study tissue-specific, steroid hormone-induced gene expression in vertebrates for decades, the mechanisms responsible for regulating this gene remain elusive. Ov is repressed in non-oviduct tissue and in estrogen-deprived oviduct by a strong repressor site located from -130 to -100 and designated CAR for COUP-TF adjacent repressor. The goal of this study was to identify the CAR binding protein(s). A transcription factor database search revealed that a putative interferon-stimulated response element (ISRE), which binds interferon regulatory factors (IRFs), is located in this region. Gel mobility shift assays demonstrated that the protein(s) binding to the CAR site is recognized by an IRF antibody and that mutations in the ISRE abolish that binding. In hopes of identifying the IRF(s) responsible for the tissue-specific regulation of Ov, mRNA levels for IRFs-4, -8, and -10 were measured in seven tissues from chicks treated with or without estrogen. PCR experiments showed that both IRF-8 and -10 are expressed in all chick tissues tested whereas IRF-4 has a much more limited expression pattern. Transfection experiments with OvCAT (chloramphenicol acetyltransferase) reporter constructs demonstrated that both IRF-4 and IRF-10 are capable of repressing the Ov gene even in the presence of steroid hormones and that nucleotides in the ISRE are required for repression. These experiments indicate that the repressor activity associated with the CAR site is mediated by IRF family members and suggest that IRF members also repress Ov in non-oviduct tissues.
| S-EPMC2749989 | biostudies-literature