E-GEOD-92314
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-92314 | ExpressionAtlas | 2020-04-15
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [RNA-Seq]
| PRJNA357201 | ENA
Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants
| PRJNA357453 | ENA
Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [Nanostring]
| PRJNA357454 | ENA
Project description:Aging is a time-dependent biological phenomenon governed by complex networks of regulatory components and their transitions over lifetime. Yet, there have been limited efforts to pin down age-associated networks and map their dynamic characteristics onto aging phenotypes. Here, we built time-course genetic regulatory networks of NAM/ATAF/CUC (NAC) transcription factors during the course of leaf aging in Arabidopsis, using causal regulatory relationships among NACs identified from mutants of 49 aging-associated NACs. These temporal networks revealed a regulatory inversion from activating to repressive regulatory modes at a pre-senescent stage. The inversion was governed by three hub NACs, and their mutants conferred earlier aging with altered expression of reactive oxygen species and salicylic acid response genes. Overexpression of the hub NACs delayed the regulatory inversion, rendering delayed age-dependent cell death. We conclude that the regulatory inversion in NAC networks at a pre-senescent stage directs when age-dependent cell death should proceed in plants.
2018-04-29 | GSE92314 | GEO
Project description:Aging is a time-dependent biological phenomenon governed by complex networks of regulatory components and their transitions over lifetime. Yet, there have been limited efforts to pin down age-associated networks and map their dynamic characteristics onto aging phenotypes. Here, we built time-course genetic regulatory networks of NAM/ATAF/CUC (NAC) transcription factors during the course of leaf aging in Arabidopsis, using causal regulatory relationships among NACs identified from mutants of 49 aging-associated NACs. These temporal networks revealed a regulatory inversion from activating to repressive regulatory modes at a pre-senescent stage. The inversion was governed by three hub NACs, and their mutants conferred earlier aging with altered expression of reactive oxygen species and salicylic acid response genes. Overexpression of the hub NACs delayed the regulatory inversion, rendering delayed age-dependent cell death. We conclude that the regulatory inversion in NAC networks at a pre-senescent stage directs when age-dependent cell death should proceed in plants.
2018-04-29 | GSE92369 | GEO
Project description:We previously identified a population of IL-10-producing, T follicular helper-like cells ("Tfh10"), linked to suppressed vaccine responses in aged mice. Here, we applied scRNA-seq and scATAC-seq to characterize Tfh10 – and the full CD4+ memory T cell (CD4+TM) compartment – in young and old mice. Unprecedented scRNA-seq coverage of the CD4+TM compartment and parallel chromatin accessibility measurements (scATAC-seq) enabled identification of 13 CD4+TM populations, which we validated as a reference through comprehensive cross-comparison to aging cell atlases and scRNA-seq studies reporting Tfh10 in other contexts. In addition, we compared sc-resolved populations to flow-sorted CD4+TM populations (Treg, Tfh10 and "nonTfh, non-Treg IL-10-") subjected to bulk RNA-seq and bulk ATAC-seq. Beyond robust characterization of age- and cell-type-dependent transcriptional landscapes, we used integrative computational modeling to predict the underlying regulatory mechanisms: We inferred gene regulatory networks (GRNs) that describe transcription-factor control of gene expression in each T-cell population and how these circuits change with age. Furthermore, we integrated our data with prior, pan-cell scRNA-seq studies to identify intercellular-signaling networks driving age-dependent changes in CD4+TM. Our atlas of finely resolved CD4+TM subsets, GRNs and cell-cell communication networks is a critical resource for analysis of biologic processes operative in memory T cells in youth and old age. The resource presents new opportunities to manipulate regulatory circuits in CD4+TM, which, long-term, could improve immune responses in the elderly.
2023-08-07 | GSE228667 | GEO
Project description:We previously identified a population of IL-10-producing, T follicular helper-like cells ("Tfh10"), linked to suppressed vaccine responses in aged mice. Here, we applied scRNA-seq and scATAC-seq to characterize Tfh10 – and the full CD4+ memory T cell (CD4+TM) compartment – in young and old mice. Unprecedented scRNA-seq coverage of the CD4+TM compartment and parallel chromatin accessibility measurements (scATAC-seq) enabled identification of 13 CD4+TM populations, which we validated as a reference through comprehensive cross-comparison to aging cell atlases and scRNA-seq studies reporting Tfh10 in other contexts. In addition, we compared sc-resolved populations to flow-sorted CD4+TM populations (Treg, Tfh10 and "nonTfh, non-Treg IL-10-") subjected to bulk RNA-seq and bulk ATAC-seq. Beyond robust characterization of age- and cell-type-dependent transcriptional landscapes, we used integrative computational modeling to predict the underlying regulatory mechanisms: We inferred gene regulatory networks (GRNs) that describe transcription-factor control of gene expression in each T-cell population and how these circuits change with age. Furthermore, we integrated our data with prior, pan-cell scRNA-seq studies to identify intercellular-signaling networks driving age-dependent changes in CD4+TM. Our atlas of finely resolved CD4+TM subsets, GRNs and cell-cell communication networks is a critical resource for analysis of biologic processes operative in memory T cells in youth and old age. The resource presents new opportunities to manipulate regulatory circuits in CD4+TM, which, long-term, could improve immune responses in the elderly.
2023-08-07 | GSE228666 | GEO
Project description:We previously identified a population of IL-10-producing, T follicular helper-like cells ("Tfh10"), linked to suppressed vaccine responses in aged mice. Here, we applied scRNA-seq and scATAC-seq to characterize Tfh10 – and the full CD4+ memory T cell (CD4+TM) compartment – in young and old mice. Unprecedented scRNA-seq coverage of the CD4+TM compartment and parallel chromatin accessibility measurements (scATAC-seq) enabled identification of 13 CD4+TM populations, which we validated as a reference through comprehensive cross-comparison to aging cell atlases and scRNA-seq studies reporting Tfh10 in other contexts. In addition, we compared sc-resolved populations to flow-sorted CD4+TM populations (Treg, Tfh10 and "nonTfh, non-Treg IL-10-") subjected to bulk RNA-seq and bulk ATAC-seq. Beyond robust characterization of age- and cell-type-dependent transcriptional landscapes, we used integrative computational modeling to predict the underlying regulatory mechanisms: We inferred gene regulatory networks (GRNs) that describe transcription-factor control of gene expression in each T-cell population and how these circuits change with age. Furthermore, we integrated our data with prior, pan-cell scRNA-seq studies to identify intercellular-signaling networks driving age-dependent changes in CD4+TM. Our atlas of finely resolved CD4+TM subsets, GRNs and cell-cell communication networks is a critical resource for analysis of biologic processes operative in memory T cells in youth and old age. The resource presents new opportunities to manipulate regulatory circuits in CD4+TM, which, long-term, could improve immune responses in the elderly.
2023-08-07 | GSE228660 | GEO
Project description:We previously identified a population of IL-10-producing, T follicular helper-like cells ("Tfh10"), linked to suppressed vaccine responses in aged mice. Here, we applied scRNA-seq and scATAC-seq to characterize Tfh10 – and the full CD4+ memory T cell (CD4+TM) compartment – in young and old mice. Unprecedented scRNA-seq coverage of the CD4+TM compartment and parallel chromatin accessibility measurements (scATAC-seq) enabled identification of 13 CD4+TM populations, which we validated as a reference through comprehensive cross-comparison to aging cell atlases and scRNA-seq studies reporting Tfh10 in other contexts. In addition, we compared sc-resolved populations to flow-sorted CD4+TM populations (Treg, Tfh10 and "nonTfh, non-Treg IL-10-") subjected to bulk RNA-seq and bulk ATAC-seq. Beyond robust characterization of age- and cell-type-dependent transcriptional landscapes, we used integrative computational modeling to predict the underlying regulatory mechanisms: We inferred gene regulatory networks (GRNs) that describe transcription-factor control of gene expression in each T-cell population and how these circuits change with age. Furthermore, we integrated our data with prior, pan-cell scRNA-seq studies to identify intercellular-signaling networks driving age-dependent changes in CD4+TM. Our atlas of finely resolved CD4+TM subsets, GRNs and cell-cell communication networks is a critical resource for analysis of biologic processes operative in memory T cells in youth and old age. The resource presents new opportunities to manipulate regulatory circuits in CD4+TM, which, long-term, could improve immune responses in the elderly.
2023-08-07 | GSE228659 | GEO
Project description:Identification of microRNA-dependent gene regulatory networks driving human pancreatic endocrine cell differentiation [small RNA-seq]
| PRJNA474511 | ENA