The difference of gene expression and splicing between the WT and scl mutants.
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryza sativa
PROVIDER: GSE307287 | GEO | 2026/08/19
REPOSITORIES: GEO
Similar Datasets
Project description:Serine/arginine-rich (SR) proteins are important splicing factors which play significant roles in spliceosome assembly and splicing regulation. However, little is known regarding their biological functions in plants. Here, we analyzed the phenotypes of mutants upon depleting different subfamilies of Arabidopsis SR proteins. We found that loss of the functions of SC35 and SC35-like (SCL) proteins cause pleiotropic changes in plant morphology and development, including serrated leaves, late flowering, shorter roots and abnormal silique phyllotaxy. Using RNA-seq, we found that SC35 and SCL proteins play roles in the pre-mRNA splicing. Motif analysis revealed that SC35 and SCL proteins preferentially bind to a specific RNA sequence containing the AGAAGA motif. In addition, the transcriptions of a subset of genes are affected by the deletion of SC35 and SCL proteins which interact with NRPB4, a specific subunit of RNA polymerase II. The splicing of FLOWERING LOCUS C (FLC) intron1 and transcription of FLC were significantly regulated by SC35 and SCL proteins to control Arabidopsis flowering. Therefore, our findings provide mechanistic insight into the functions of plant SC35 and SCL proteins in the regulation of splicing and transcription to maintain the proper expression of genes and development.
2017-01-26 | GSE93910 | GEO
Project description:We investigated the function of the plant-specific SR protein SC106 in pre-mRNA splicing regulation and abiotic stress responses in rice. The loss-of-function mutant, SC106, showed increased sensitivity to salt. We performed genome-wide analyses of gene expression and splicing in seedlings subjected to salt stress and identified multiple splice isoforms from stress-responsive genes dependent on SC106.
2023-10-26 | GSE232160 | GEO
Project description:Mammalian SR proteins are a family of reversibly phosphorylated RNA binding proteins primarily studied for their roles in alternative splicing. While budding yeast lack alternative splicing, they do have three SR-like proteins: Npl3, Gbp2, and Hrb1. However, these have been primarily studied for their roles in mRNA export, leaving their potential roles in splicing largely unexplored. Here we combined high-density genetic interaction profiling and genome-wide splicing-sensitive microarray analysis to demonstrate that a single SR-like protein, Npl3, is required for efficient splicing of a large set of pre-mRNAs in Saccharomyces cerevisiae. We tested the hypothesis that Npl3 promotes splicing by facilitating co-transcriptional recruitment of splicing factors. Using chromatin immunoprecipitation, we showed that mutation of NPL3 reduces the occupancy of U1 and U2 snRNPs at Npl3-stimulated genes. This provides the first evidence that an SR protein can promote recruitment of splicing factors to chromatin.
2008-12-31 | GSE11491 | GEO
Project description:Understanding the molecular basis of cell fate decision is critical to shed light onto biological processes supporting tissue formation. In particular, whether lineage-fated cells derive from multi-primed progenitors and need to establish active fate restriction mechanisms to engage in a differentiation pathway is still matter of debate. To characterise the mechanisms underlying specification of blood-fated cells from mesodermal precursors, we studied the transcriptional activity of the key hematopoietic regulator SCL/TAL1. Scl-null mouse embryos die at embryonic day E9.5 from absence of blood formation, and exhibit mis-specification of mesodermal cells into cardiomyocytes, thus offering an excellent entry point for mechanistic studies of fate determination. Using high-throughput assays from mouse ES cell-derived mesodermal cells, we showed that, in parallel with activating the blood program and repressing the cardiac and paraxial programs, SCL strongly activates expression of repressors, such as ETO2 (known partner of SCL) and RYBP (member of Polycomb repressive complex PRC1). ETO2’s association with chromatin reflects SCL’s overall genomic binding, pointing to ETO2’s modulatory, rather than purely repressive, transcriptional activities. In contrast, SCL/RYBP chromatin co-occupancy is preferentially enriched at genes normally repressed in blood-fated cells and involved in early developmental processes and alternative lineages, highlighting a relationship between SCL and RYBP/PRC1 in repressive processes. Remarkably, SCL is critical for maintaining high levels of PRC1-associated repressive histone mark H2AK119ub genome-wide. It is also required for maximal levels of repressive mark H3K27me3 on genes normally repressed. Finally, Rybp knock-down in differentiating ES cells phenocopies the cardiac phenotype of Scl-null cells, supporting a functional interaction between SCL and a critical repressive chromatin remodeling complex. Altogether, these data unveil the establishment of a repressive environment in mesodermal progenitors by a hematopoietic-specific transcriptional regulator. This leads to restriction of expression of regulators of alternative fates and uncompromised commitment towards a hematopoietic identity.
2018-12-27 | GSE104844 | GEO
Project description:Mammalian SR proteins are a family of reversibly phosphorylated RNA binding proteins primarily studied for their roles in alternative splicing. While budding yeast lack alternative splicing, they do have three SR-like proteins: Npl3, Gbp2, and Hrb1. However, these have been primarily studied for their roles in mRNA export, leaving their potential roles in splicing largely unexplored. Here we combined high-density genetic interaction profiling and genome-wide splicing-sensitive microarray analysis to demonstrate that a single SR-like protein, Npl3, is required for efficient splicing of a large set of pre-mRNAs in Saccharomyces cerevisiae. We tested the hypothesis that Npl3 promotes splicing by facilitating co-transcriptional recruitment of splicing factors. Using chromatin immunoprecipitation, we showed that mutation of NPL3 reduces the occupancy of U1 and U2 snRNPs at Npl3-stimulated genes. This provides the first evidence that an SR protein can promote recruitment of splicing factors to chromatin. Splicing-specific microarrays were used to assay changes to splicing in single and double deletion mutants of non-essential SR proteins, in a deletion mutant of a non-essential component of the nonsense-mediated decay pathway, and in a double deletion mutant of in an SR protein plus a non-sense mediated decay factor in Saccharomyces cerevisiae. The data includes both samples obtained at the permissive temperature and also shifts to the non-permissive temperature for some mutants, as well as dye-flipped technical replicates.
2008-12-30 | E-GEOD-11491 | biostudies-arrayexpress
Project description:Here, we investigated the function of the plant-specific SR protein RS33 in pre-mRNA splicing regulation and abiotic stress responses in rice. The loss-of-function mutant, rs33, showed increased sensitivity to salt and low-temperature stress. Genome-wide analyses of gene expression and splicing in seedlings subjected to these stresses identified multiple splice isoforms from stress-responsive genes dependent on RS33. The number of RS33-regulated genes is much higher under low-temperature stress as compared to salt stress. Our results suggest that this plant-specific splicing factor plays crucial and distinct roles during plant adaptation to abiotic stresses.
2022-06-15 | GSE194283 | GEO
Project description:Alternative splicing (AS) of pre-mRNA is utilized by higher eukaryotes to achieve increased transcriptome and proteomic complexity. The serine/arginine (SR) splicing factors regulate tissue- or cell type-specific AS in a concentration and phosphorylation dependent manner. However, the mechanisms that modulate the cellular levels of active SR proteins remain to be elucidated. In the present study, we provide evidence for a role for the long nuclear-retained regulatory RNA (nrRNA), MALAT1 in AS regulation. MALAT1 interacts with SR proteins and influences the distribution of these and other splicing factors in nuclear speckle domains. Depletion of MALAT1 changes AS of endogenous pre-mRNAs, similar to what was observed upon overexpression of SR proteins. Furthermore, MALAT1 regulates cellular levels of phosphorylated forms of SR proteins. Taken together, our results suggest that MALAT1 regulates AS by modulating the levels of active SR proteins. Our results further highlight a novel role for a nrRNA in the regulation of gene expression. Malat1 Antisense and control knockdowns evaluated on a microarray platform to profile alternative splicing levels for 5782 cassette-type alternative exons.
2010-09-01 | E-GEOD-22963 | biostudies-arrayexpress
Project description:Endothelium in embryonic hematopoietic tissues generates hematopoietic stem/progenitor cells; however, it is unknown how its unique potential is specified. We show that transcription factor Scl/Tal1 is essential for both establishing the hematopoietic transcriptional program in hemogenic endothelium and preventing its misspecification to a cardiomyogenic fate. Scl-/- embryos activated a cardiac transcriptional program in yolk sac endothelium, leading to the emergence of CD31+Pdgfrα+ cardiogenic precursors that generated spontaneously beating cardiomyocytes. Ectopic cardiogenesis was also observed in Scl-/- hearts, where the disorganized endocardium precociously differentiated into cardiomyocytes. Induction of mosaic deletion of Scl in Sclfl/flRosa26Cre-ERT2 embryos revealed a cell-intrinsic, temporal requirement for Scl to prevent cardiomyogenesis from endothelium. Scl-/- endothelium also upregulated the expression of Wnt antagonists, which promoted rapid cardiomyocyte differentiation of ectopic cardiogenic cells. These results reveal unexpected plasticity in embryonic endothelium such that loss of a single master regulator can induce ectopic cardiomyogenesis from endothelial cells.
2012-08-03 | GSE27445 | GEO
Project description:Understanding the molecular basis of cell fate decision is critical to shed light onto biological processes supporting tissue formation. In particular, whether lineage-fated cells derive from multi-primed progenitors and need to establish active fate restriction mechanisms to engage in a differentiation pathway is still matter of debate. To characterise the mechanisms underlying specification of blood-fated cells from mesodermal precursors, we studied the transcriptional activity of the key hematopoietic regulator SCL/TAL1. Scl-null mouse embryos die at embryonic day E9.5 from absence of blood formation, and exhibit mis-specification of mesodermal cells into cardiomyocytes, thus offering an excellent entry point for mechanistic studies of fate determination. Using high-throughput assays from mouse ES cell-derived mesodermal cells, we showed that, in parallel with activating the blood program and repressing the cardiac and paraxial programs, SCL strongly activates expression of repressors, such as ETO2 (known partner of SCL) and RYBP (member of Polycomb repressive complex PRC1). ETO2’s association with chromatin reflects SCL’s overall genomic binding, pointing to ETO2’s modulatory, rather than purely repressive, transcriptional activities. In contrast, SCL/RYBP chromatin co-occupancy is preferentially enriched at genes normally repressed in blood-fated cells and involved in early developmental processes and alternative lineages, highlighting a relationship between SCL and RYBP/PRC1 in repressive processes. Remarkably, SCL is critical for maintaining high levels of PRC1-associated repressive histone mark H2AK119ub genome-wide. It is also required for maximal levels of repressive mark H3K27me3 on genes normally repressed. Finally, Rybp knock-down in differentiating ES cells phenocopies the cardiac phenotype of Scl-null cells, supporting a functional interaction between SCL and a critical repressive chromatin remodeling complex. Altogether, these data unveil the establishment of a repressive environment in mesodermal progenitors by a hematopoietic-specific transcriptional regulator. This leads to restriction of expression of regulators of alternative fates and uncompromised commitment towards a hematopoietic identity.
2018-12-27 | GSE104834 | GEO
Project description:Understanding the molecular basis of cell fate decision is critical to shed light onto biological processes supporting tissue formation. In particular, whether lineage-fated cells derive from multi-primed progenitors and need to establish active fate restriction mechanisms to engage in a differentiation pathway is still matter of debate. To characterise the mechanisms underlying specification of blood-fated cells from mesodermal precursors, we studied the transcriptional activity of the key hematopoietic regulator SCL/TAL1. Scl-null mouse embryos die at embryonic day E9.5 from absence of blood formation, and exhibit mis-specification of mesodermal cells into cardiomyocytes, thus offering an excellent entry point for mechanistic studies of fate determination. Using high-throughput assays from mouse ES cell-derived mesodermal cells, we showed that, in parallel with activating the blood program and repressing the cardiac and paraxial programs, SCL strongly activates expression of repressors, such as ETO2 (known partner of SCL) and RYBP (member of Polycomb repressive complex PRC1). ETO2’s association with chromatin reflects SCL’s overall genomic binding, pointing to ETO2’s modulatory, rather than purely repressive, transcriptional activities. In contrast, SCL/RYBP chromatin co-occupancy is preferentially enriched at genes normally repressed in blood-fated cells and involved in early developmental processes and alternative lineages, highlighting a relationship between SCL and RYBP/PRC1 in repressive processes. Remarkably, SCL is critical for maintaining high levels of PRC1-associated repressive histone mark H2AK119ub genome-wide. It is also required for maximal levels of repressive mark H3K27me3 on genes normally repressed. Finally, Rybp knock-down in differentiating ES cells phenocopies the cardiac phenotype of Scl-null cells, supporting a functional interaction between SCL and a critical repressive chromatin remodeling complex. Altogether, these data unveil the establishment of a repressive environment in mesodermal progenitors by a hematopoietic-specific transcriptional regulator. This leads to restriction of expression of regulators of alternative fates and uncompromised commitment towards a hematopoietic identity.
2018-12-27 | GSE104846 | GEO