Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA223668 | ENA |
REPOSITORIES: ENA
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Project description:Proper cell wall regulation is essential for growth and development in plants. Here we report that the constitutive expression of MYB87 chimera repressor causes the suppressed longitudinal organ elongation in almost all organs. Aberrant transversal growth is also observed in multiple organs which coincide with transversally expanded or swollen cells. Microarray analysis revealed the transcript levels of various primary cell wall related enes are up- or down-regulated, and those of secondary wall related genes are down- regulated in the chimera repressor plants. These findings ontribute to the further understanding of complex cell wall regulations and their roles in plant growth and development. Transcriptomes of 35S:MYB87-SRDX and wild-type Arabidopsis seedling were compared.
2014-03-05 | E-GEOD-51595 | biostudies-arrayexpress
Project description:Proper cell wall regulation is essential for growth and development in plants. Here we report that the constitutive expression of MYB87 chimera repressor causes the suppressed longitudinal organ elongation in almost all organs. Aberrant transversal growth is also observed in multiple organs which coincide with transversally expanded or swollen cells. Microarray analysis revealed the transcript levels of various primary cell wall related enes are up- or down-regulated, and those of secondary wall related genes are down- regulated in the chimera repressor plants. These findings ontribute to the further understanding of complex cell wall regulations and their roles in plant growth and development.
2014-03-05 | GSE51595 | GEO
Project description:We cloned and characterized a subgroup S4 R2R3 Myb transcription factor, PgMyb308-like. Overexpressing PgMyb308-like in pomegranate hairy roots. Transcriptome analysis of PgMyb308-like-overexpressing hairy roots revealed reprogramming of cell wall-related genes, while overexpression of PgMyb308-like in Arabidopsis thaliana plants uncovered its distinct role in a different genetic and metabolic background. The results suggest that PgMyb308-like activates genes in the shikimate pathway and lignin biosynthesis, but suppresses those involved in the production of HTs and flavonoids.
2022-05-25 | GSE178072 | GEO
Project description:Light and brassinosteroids (BRs) have been proved to be crucial in regulating plant growth and development, however, the mechanism of how they synergistically function is still largely unknown. To explore the underlying mechanisms in photomorphogenesis, genome-wide analyses were carried out through examining the gene expressions of the dark-grown WT or BR biosynthesis-defective mutant det2 seedlings in presence of light stimuli, or exogenous Brassinolide (BL). Results showed that BR deficiency stimulates, while BL treatment suppresses, the expressions of light responsive genes and photomorphogenesis, revealing the negative effects of BR in photomorphogenesis. This is consistent with that genes involved in cell wall modification and cellular metabolism were specifically modulated by BL during dark-light transition, and altered expressions of genes related to energy utilization. Further analysis revealed that hormone biosynthesis and signaling related genes, especially those of auxin, were altered under BL treatment or light stimuli, indicating that BR may modulate photomorphogenesis through synergetic regulation with other hormones. Additionally, suppressed ubiquitin-cycle pathway during light-dark transition hinted the presence of a complicated network among light, hormone and protein degradation. The study provides the direct evidence of BR effects in photomorphogenesis and identified the genes involved in BR and light signaling pathway, which will help to elucidate the molecular mechanism of plant photomorphogenesis. In order to study how BR involves in photomorphogenesis, dark-grown wild-type or BR- deficient mutant det2 seedlings were treated with BL or light, gene expression pattern analysis confirmed that BR deficiency specifically induces, while BL treatment suppresses, the expression of photosynthesis and light responsive genes. Interplay of BR and other hormones play important roles in dark-light transition and photomorphogenesis. CEL files for the wildtype samples are lost. 14 samples were analysised and including repeats.
2010-02-22 | E-GEOD-14788 | biostudies-arrayexpress
Project description:Light and brassinosteroids (BRs) have been proved to be crucial in regulating plant growth and development, however, the mechanism of how they synergistically function is still largely unknown. To explore the underlying mechanisms in photomorphogenesis, genome-wide analyses were carried out through examining the gene expressions of the dark-grown WT or BR biosynthesis-defective mutant det2 seedlings in presence of light stimuli, or exogenous Brassinolide (BL). Results showed that BR deficiency stimulates, while BL treatment suppresses, the expressions of light responsive genes and photomorphogenesis, revealing the negative effects of BR in photomorphogenesis. This is consistent with that genes involved in cell wall modification and cellular metabolism were specifically modulated by BL during dark-light transition, and altered expressions of genes related to energy utilization. Further analysis revealed that hormone biosynthesis and signaling related genes, especially those of auxin, were altered under BL treatment or light stimuli, indicating that BR may modulate photomorphogenesis through synergetic regulation with other hormones. Additionally, suppressed ubiquitin-cycle pathway during light-dark transition hinted the presence of a complicated network among light, hormone and protein degradation. The study provides the direct evidence of BR effects in photomorphogenesis and identified the genes involved in BR and light signaling pathway, which will help to elucidate the molecular mechanism of plant photomorphogenesis.
2010-02-10 | GSE14788 | GEO
Project description:The cell wall is a crucial structure in plant cells, and modifications in its composition often have a major impact on growth and development. However, the molecular mechanisms responsible for the negative effects of cell wall alterations on plant growth are largely unknown. It was previously shown that a reduction in the levels of de-esterified homogalacturonan, a major pectin component of cell walls, in Arabidopsis thaliana plants expressing a fungal polygalacturonase or mutated in the QUASIMODO2 gene (qua2-1 plants), cause severe growth defects. Here we show that the class III peroxidase AtPrx71 is strongly up-regulated in these plants, as well as in response to alterations of other wall structural components, including treatments the cellulose synthase inhibitor isoxaben. Analysis of atprx71 loss-of-function mutants and of plants overexpressing AtPrx71 indicates that this gene negatively affects Arabidopsis growth at different stages of development. Furthermore, lack of AtPrx71 partially suppresses the dwarf phenotype of qua2-1, suggesting that this protein contributes to the growth defects observed in plants undergoing cell wall damage. AtPrx71 appears to promote the production of reactive oxygen species in qua2-1 plants, as well as in plants treated with isoxaben. We propose that production of reactive oxygen species mediated by AtPrx71 negatively regulates Arabidopsis growth both during physiological development and in response to loss of cell wall integrity. Transcriptional profiling of Arabidopsis thaliana wt control plants and PG57 and PG26 transgenic lines overexpressing the AtPrx71 gene.
2016-01-06 | E-GEOD-66980 | biostudies-arrayexpress
Project description:Development of cancer is intimately associated with genetic abnormalities that target proteins with intrinsically disordered regions (IDRs). In human hematological malignancies, recurrent chromosomal translocation of nucleoporin (NUP98 or NUP214) generates an aberrant chimera that invariably retains nucleoporin’s IDR, tandemly dispersed phenylalanine-andglycine (FG) repeats1-3. However, it remains largely elusive how unstructured IDRs contribute to oncogenesis. We here show that IDR or FG repeats harbored within NUP98-HOXA9, a homeodomain-containing transcription factor (TF) chimera recurrently detected in acute leukemia patients1,4,5, is essential for establishing nuclear liquid-liquid phase separation (LLPS) puncta and for inducing leukemic transformation of primary hematopoietic cells in vitro and in vivo. Strikingly, LLPS of NUP98-HOXA9 not only promotes chromatin occupancy of chimera TF oncoproteins but is also required for formation of a broad, ‘super-enhancer’-like binding pattern, typically seen at a battery of leukemia-related loci exemplified by HOX, MEIS and PBX genes, potentiating their transcriptional activation. An artificial HOX chimera, created by replacing NUP98’s FG repeats with an unrelated LLPSforming IDR of FUS6,7, had similar enhancement effects on chimera’s chromatin binding and target gene activation. Via Hi-C mapping, we further demonstrated that the phase-separated NUP98-HOXA9 protein assembly is able to induce formation of CTCF-independent chromatin looping enriched at leukemic oncogenes. Together, this report describes a proof-of-principle example wherein cancer acquires mutation to establish condensates of oncogenic TFs via a phase separation mechanism, which simultaneously enhances their chromatin targeting and induces organization of aberrant three-dimensional chromatin structure during tumorous transformation. As a range of LLPS-competent molecules are implicated in various human cancers, this mechanism can potentially be generalized to many malignant and diseased settings.
2021-04-22 | PXD023548 | Pride
Project description:Plant cell walls are complex structures that contain a matrix of cellulose, lignin and hemicellulose. The regulation of the biosynthesis of these components has been well-studied in the eudicot plant Arabidopsis thaliana, and a transcriptional network has been elucidated. Several NAC and MYB family transcription factors are key regulators of secondary cell wall biosynthesis, and their functional characterization provides significant insight into the complex underlying transcriptional network. Genetic and structural evidence suggests that genes controlling this process might be different between eudicots and monocots. Here, the model grass Brachypodium distachyon has been selected to characterize the function of GNRF (GRASS NAC REPRESSOR OF FLOWERING), SWAM1 (SECONDARY WALL ASSOCIATED MYB1), and SWAM4 in the regulation of secondary cell wall biosynthesis. Functional characterization was performed by using the overexpression plants GNRF-OE and SWAM4-OE; sodium azide mutant plants from a TILLING (Targeting Induced Local Lesion IN Genome) collection for gnrf-1, gnrf-2, gnrf-3, gnrf-4, gnrf-5, swam4-1, and swam4-2; a T-DNA insertional mutant plant, gnrf-6; and a dominant repressor plant, SWAM4-DR. GNRF-OE plants remained at juvenile stage and exhibited persistent vegetative growth, and some gnrf mutant plants were late flowering. SWAM4-DR plants were severely dwarfed. Stems of all genotypes mentioned above were subjected to RNA-seq analysis.
2019-08-02 | E-MTAB-8172 | biostudies-arrayexpress
Project description:Development of cancer is intimately associated with genetic abnormalities that target proteins with intrinsically disordered regions (IDRs). In human hematological malignancies, recurrent chromosomal translocation of nucleoporin (NUP98 or NUP214) generates an aberrant chimera that invariably retains nucleoporin?s IDR, tandemly dispersed phenylalanine-and-glycine (FG) repeats. However, it remains elusive how unstructured IDRs contribute to oncogenesis. We show that IDR harbored within NUP98-HOXA9, a homeodomain-containing transcription factor (TF) chimera recurrently detected in leukemias, is essential for establishing liquid-liquid phase separation (LLPS) puncta of chimera and for inducing leukemic transformation. Strikingly, LLPS of NUP98-HOXA9 not only promotes chromatin occupancy of chimera TFs but is also required for formation of a broad, ?super-enhancer?-like binding pattern, typically seen at a battery of leukemogenic genes, potentiating their transcriptional activation. Artificial HOX chimera (FUS-HOXA9), created by replacing NUP98?s FG repeats with an unrelated LLPS-forming IDR of FUS, had similar enhancement effects on chimera?s genome-wide binding and target gene activation. Hi-C mapping further demonstrated that phase-separated NUP98-HOXA9 induces CTCF-independent chromatin looping enriched at proto-oncogenes. Together, this report describes a proof-of-principle example wherein cancer acquires mutation to establish oncogenic TF condensates via phase separation, which simultaneously enhances their genomic targeting and induces organization of aberrant three-dimensional chromatin structure during tumorous transformation. As LLPS-competent molecules are frequently implicated in diseases, this mechanism can potentially be generalized to many malignant and pathological settings.
2021-04-19 | GSE144642 | GEO
Project description:Development of cancer is intimately associated with genetic abnormalities that target proteins with intrinsically disordered regions (IDRs). In human hematological malignancies, recurrent chromosomal translocation of nucleoporin (NUP98 or NUP214) generates an aberrant chimera that invariably retains nucleoporin?s IDR, tandemly dispersed phenylalanine-and-glycine (FG) repeats. However, it remains elusive how unstructured IDRs contribute to oncogenesis. We show that IDR harbored within NUP98-HOXA9, a homeodomain-containing transcription factor (TF) chimera recurrently detected in leukemias, is essential for establishing liquid-liquid phase separation (LLPS) puncta of chimera and for inducing leukemic transformation. Strikingly, LLPS of NUP98-HOXA9 not only promotes chromatin occupancy of chimera TFs but is also required for formation of a broad, ?super-enhancer?-like binding pattern, typically seen at a battery of leukemogenic genes, potentiating their transcriptional activation. Artificial HOX chimera (FUS-HOXA9), created by replacing NUP98?s FG repeats with an unrelated LLPS-forming IDR of FUS, had similar enhancement effects on chimera?s genome-wide binding and target gene activation. Hi-C mapping further demonstrated that phase-separated NUP98-HOXA9 induces CTCF-independent chromatin looping enriched at proto-oncogenes. Together, this report describes a proof-of-principle example wherein cancer acquires mutation to establish oncogenic TF condensates via phase separation, which simultaneously enhances their genomic targeting and induces organization of aberrant three-dimensional chromatin structure during tumorous transformation. As LLPS-competent molecules are frequently implicated in diseases, this mechanism can potentially be generalized to many malignant and pathological settings.
2021-04-19 | GSE144076 | GEO