Background: Skewing root patterns provide key insights into root growth strategies and mechanism that produce root architectures Roots exhibit skewing and waving when grown on a tilted, impenetrable surface, and while the genetics guiding these morphologies have been examined, the underlying molecular mechanisms of skewing and waving remain unclear. In this study, transcriptome data were derived from two Arabidopsis ecotypes, WS and Col-0, under three tilted growth conditions in order to identify candidate genes involved in skewing. WS is a skewing ecotype. Col-0 is a non-skewing ecotype. Results: This work identifies a number of genes that are likely involved in skewing, using growth conditions that differentially affect skewing and waving. Comparing the gene expression profiles of WS and Col-0 in different tilted growth conditions identified 11 candidate genes as potentially involved in the control of skewing. These 11 genes are involved in several different cellular processes, including sugar transport, salt signaling, cell wall organization, and hormone signaling. Conclusions: Many of the 11 identified genes are involved in signaling and perception, rather than the physical restructuring of roots, leading to the conclusion that root skewing is enabled through diverse environmental signaling pathways. These findings revealed further insights into the molecular mechanisms behind root skewing.
Skewing in Arabidopsis roots involves disparate environmental signaling pathways.
Age, Specimen part
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A transcriptional repressor co-regulatory network governing androgen response in prostate cancers.
Specimen part, Cell line, Treatment
View SamplesDeregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. However, the exact mechanics and the functional consequences associated with this crosstalk between ERG and AR still remains relatively unknown. Interestingly, through chromatin immunoprecipitation coupled with massively parallel sequencing, we discover that ERG and other commonly over-expressed transcriptional co-repressors (HDAC1, HDAC2, HDAC3 and EZH2) are wired into an AR-centric transcriptional network via a spectrum of distal enhancers and/or proximal promoters. We show that ERG represses several AR target genes involved in epithelial differentiation. Furthermore, we demonstrated that suppression of the androgen-induced gene, Vinculin, by ERG and histone deacetylases increases cancer cell invasiveness. From our results, we propose that ERG, histone deactelyases and the histone methyltransferase, EZH2, could impede epithelial differentiation and contribute to prostate cancer progression, in part through modulating the transcriptional output of AR.
A transcriptional repressor co-regulatory network governing androgen response in prostate cancers.
Specimen part, Cell line, Treatment
View SamplesDeregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. However, the exact mechanics and the functional consequences associated with this crosstalk between ERG and AR still remains relatively unknown. Interestingly, through chromatin immunoprecipitation coupled with massively parallel sequencing, we discover that ERG and other commonly over-expressed transcriptional co-repressors (HDAC1, HDAC2, HDAC3 and EZH2) are wired into an AR centric transcriptional network via a spectrum of distal enhancers and/or proximal promoters. We show that ERG represses several AR target genes involved in epithelial differentiation. Furthermore, we demonstrated that suppression of the androgen induced gene, Vinculin, by ERG and histone deacetylases increases cancer cell invasiveness. From our results, we propose that ERG, histone deactelyases and the histone methyltransferase, EZH2, could impede epithelial differentiation and contribute to prostate cancer progression, in part through modulating the transcriptional output of AR.
A transcriptional repressor co-regulatory network governing androgen response in prostate cancers.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.
Specimen part
View SamplesThis study aims to look at gene expresion profiles between wildtype and Sox9 knockout cells of the vertebral column in a E12.5 mouse embryo. Instead of looking at the whole vertebral column, only cells expressing Sox9 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.
In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.
Specimen part
View SamplesThis study aims to look at gene expresion profiles between wildtype and Bapx1 knockout cells of the hindlimbs in a E12.5 mouse embryo. Instead of looking at the whole hindlimbs,only cells expressing Bapx1 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.
In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.
Specimen part
View SamplesThis study aims to look at gene expresion profiles between wildtype and Bapx1 knockout cells of the vertebral column in a E12.5 mouse embryo. Instead of looking at the whole vertebral column ,only cells expressing Bapx1 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.
In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.
Specimen part
View SamplesThis study aims to look at gene expresion profiles between wildtype and Bapx1 knockout cells of the spleen in a E12.5 mouse embryo. Instead of looking at the whole spleen,only cells expressing Bapx1 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.
In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.
Specimen part
View SamplesThis study aims to look at gene expresion profiles between wildtype and Bapx1 knockout cells of the forelimbs in a E12.5 mouse embryo. Instead of looking at the whole forelimbs, only cells expressing Bapx1 were sorted by Fluroscent Activated Cell Sorting (FACS) and subjected to expression profiling by microarray.
In vivo genome-wide analysis of multiple tissues identifies gene regulatory networks, novel functions and downstream regulatory genes for Bapx1 and its co-regulation with Sox9 in the mammalian vertebral column.
Specimen part
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