Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4
Ontology highlight
ABSTRACT: To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans. Three replicates comparing RNA from sma-2(e502) L4 whole animal with RNA from wild-type L4 whole animal, in which one is dye flipped. Plus one array comparing RNA from sma-4(e729) L4 whole animal with RNA from wild-type L4 whole animal.
Project description:Reproductive cessation is perhaps the earliest aging phenotypes humans experience. Similarly, C. elegans' reproduction ceases in mid-adulthood. Although somatic aging has been studied in both worms and humans, mechanisms regulating reproductive aging are not yet understood. Here we show that TGF-beta Sma/Mab activity regulates reproductive aging transcriptionally separable from its regulation of body size growth. This SuperSeries is composed of the following subset Series: GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4 Refer to individual Series
Project description:To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. Eight replicates comparing RNA from oocyte samples collected from day 8 sma-2(e502);fem-1(hc17) animals with RNA from oocyte samples collected from day 8 fem-1(hc17) animals. Five out of eight are dye-flipped.
Project description:Microarray data for study "The master regulators AphA and LuxR control the Vibrio harveyi quorum-sensing regulon: analysis of their individual and combined effects". Bacteria use a chemical communication process called quorum sensing to control transitions between individual and group behaviors. In the Vibrio harveyi quorum-sensing circuit, two master transcription factors AphA and LuxR coordinate the quorum-sensing response. Here we show that AphA regulates 167 genes, LuxR regulates 625 genes, and they co-regulate 77 genes. LuxR strongly controls genes both at low-cell-density and high-cell-density, suggesting it is the major quorum-sensing regulator. By contrast, AphA is absent at high-cell-density, and acts to fine-tune quorum-sensing gene expression at low-cell-density. We examined two loci as case studies of co-regulation by AphA and LuxR. First, AphA and LuxR directly regulate expression of the genes encoding the quorum regulatory small RNAs Qrr2, Qrr3, and Qrr4, the consequence of which is a specifically timed transition between the individual and the group lifestyle. Second, AphA and LuxR repress type III secretion system genes but at different times and to different extents. The consequence of this regulation is that type III secretion is restricted to a peak at mid-cell-density. Thus, asymmetric production of AphA and LuxR coupled with differences in their strength and timing of target gene regulation generates a precise temporal pattern of gene expression. Triplicate biological samples of Vibrio harveyi strains BB721 and JAF548 were hybridized to Agilent arrays (Amadid design ID: 037644), and one experiment was a control dye-swap, for a total of four experiments in this array set.
Project description:Microarray data for study "The master regulators AphA and LuxR control the Vibrio harveyi quorum-sensing regulon: analysis of their individual and combined effects". Bacteria use a chemical communication process called quorum sensing to control transitions between individual and group behaviors. In the Vibrio harveyi quorum-sensing circuit, two master transcription factors AphA and LuxR coordinate the quorum-sensing response. Here we show that AphA regulates 167 genes, LuxR regulates 625 genes, and they co-regulate 77 genes. LuxR strongly controls genes both at low-cell-density and high-cell-density, suggesting it is the major quorum-sensing regulator. By contrast, AphA is absent at high-cell-density, and acts to fine-tune quorum-sensing gene expression at low-cell-density. We examined two loci as case studies of co-regulation by AphA and LuxR. First, AphA and LuxR directly regulate expression of the genes encoding the quorum regulatory small RNAs Qrr2, Qrr3, and Qrr4, the consequence of which is a specifically timed transition between the individual and the group lifestyle. Second, AphA and LuxR repress type III secretion system genes but at different times and to different extents. The consequence of this regulation is that type III secretion is restricted to a peak at mid-cell-density. Thus, asymmetric production of AphA and LuxR coupled with differences in their strength and timing of target gene regulation generates a precise temporal pattern of gene expression. Triplicate biological samples of Vibrio harveyi strains STR416 and JV55 were hybridized to Agilent arrays (Amadid design ID: 021087), and one experiment was a control dye-swap, for a total of four experiments in this array set.
Project description:Microarray data for study "The master regulators AphA and LuxR control the Vibrio harveyi quorum-sensing regulon: analysis of their individual and combined effects". Bacteria use a chemical communication process called quorum sensing to control transitions between individual and group behaviors. In the Vibrio harveyi quorum-sensing circuit, two master transcription factors AphA and LuxR coordinate the quorum-sensing response. Here we show that AphA regulates 167 genes, LuxR regulates 625 genes, and they co-regulate 77 genes. LuxR strongly controls genes both at low-cell-density and high-cell-density, suggesting it is the major quorum-sensing regulator. By contrast, AphA is absent at high-cell-density, and acts to fine-tune quorum-sensing gene expression at low-cell-density. We examined two loci as case studies of co-regulation by AphA and LuxR. First, AphA and LuxR directly regulate expression of the genes encoding the quorum regulatory small RNAs Qrr2, Qrr3, and Qrr4, the consequence of which is a specifically timed transition between the individual and the group lifestyle. Second, AphA and LuxR repress type III secretion system genes but at different times and to different extents. The consequence of this regulation is that type III secretion is restricted to a peak at mid-cell-density. Thus, asymmetric production of AphA and LuxR coupled with differences in their strength and timing of target gene regulation generates a precise temporal pattern of gene expression. Triplicate biological samples of Vibrio harveyi strains KM810 and JV55 were hybridized to Agilent arrays (Amadid design ID: 021087), and one experiment was a control dye-swap, for a total of four experiments in this array set. KM810 contains a luxO D47E phosphomimic allele and a deletion in luxR; JV55 contains a luxO D47E phosphomimic allele and deletions in luxR and aphA.
Project description:Microarray data for study "The master regulators AphA and LuxR control the Vibrio harveyi quorum-sensing regulon: analysis of their individual and combined effects". Bacteria use a chemical communication process called quorum sensing to control transitions between individual and group behaviors. In the Vibrio harveyi quorum-sensing circuit, two master transcription factors AphA and LuxR coordinate the quorum-sensing response. Here we show that AphA regulates 167 genes, LuxR regulates 625 genes, and they co-regulate 77 genes. LuxR strongly controls genes both at low-cell-density and high-cell-density, suggesting it is the major quorum-sensing regulator. By contrast, AphA is absent at high-cell-density, and acts to fine-tune quorum-sensing gene expression at low-cell-density. We examined two loci as case studies of co-regulation by AphA and LuxR. First, AphA and LuxR directly regulate expression of the genes encoding the quorum regulatory small RNAs Qrr2, Qrr3, and Qrr4, the consequence of which is a specifically timed transition between the individual and the group lifestyle. Second, AphA and LuxR repress type III secretion system genes but at different times and to different extents. The consequence of this regulation is that type III secretion is restricted to a peak at mid-cell-density. Thus, asymmetric production of AphA and LuxR coupled with differences in their strength and timing of target gene regulation generates a precise temporal pattern of gene expression. Triplicate biological samples of Vibrio harveyi strains STR415 and JV54 were hybridized to Agilent arrays (Amadid design ID: 021087), and one experiment was a control dye-swap, for a total of four experiments in this array set.
Project description:Microarray data for study "The master regulators AphA and LuxR control the Vibrio harveyi quorum-sensing regulon: analysis of their individual and combined effects". Bacteria use a chemical communication process called quorum sensing to control transitions between individual and group behaviors. In the Vibrio harveyi quorum-sensing circuit, two master transcription factors AphA and LuxR coordinate the quorum-sensing response. Here we show that AphA regulates 167 genes, LuxR regulates 625 genes, and they co-regulate 77 genes. LuxR strongly controls genes both at low-cell-density and high-cell-density, suggesting it is the major quorum-sensing regulator. By contrast, AphA is absent at high-cell-density, and acts to fine-tune quorum-sensing gene expression at low-cell-density. We examined two loci as case studies of co-regulation by AphA and LuxR. First, AphA and LuxR directly regulate expression of the genes encoding the quorum regulatory small RNAs Qrr2, Qrr3, and Qrr4, the consequence of which is a specifically timed transition between the individual and the group lifestyle. Second, AphA and LuxR repress type III secretion system genes but at different times and to different extents. The consequence of this regulation is that type III secretion is restricted to a peak at mid-cell-density. Thus, asymmetric production of AphA and LuxR coupled with differences in their strength and timing of target gene regulation generates a precise temporal pattern of gene expression. Triplicate biological samples of Vibrio harveyi strains KM808 and JV54 were hybridized to Agilent arrays (Amadid design ID: 021087), and one experiment was a control dye-swap, for a total of four experiments in this array set.
Project description:To find genes in C. elegans oocytes associated with reproductive aging. Five replicates comparing RNA from oocyte samples collected from day 3 fem-1(hc17) animals with RNA from oocyte samples collected from day 8 fem-1(hc17) animals. Three out of five are dye-flipped.
Project description:The Target Of Rapamycin (TOR) protein is a Ser/Thr kinase that functions in two distinct multiprotein complexes: TORC1 and TORC2. These conserved complexes regulate many different aspects of cell growth in response to intra- and extracellular cues. Here we report the first bona fide substrate of yeast TORC1: the AGC-kinase Sch9. Six amino acids in the c-terminus of Sch9 are directly phosphorylated by TORC1. Phosphorylation of these residues is lost upon rapamycin-treatment as well as carbon- or nitrogen-starvation and transiently reduced following application of osmotic, oxidative or thermal stress. TORC1-dependent phosphorylation is required for Sch9 activity and replacement of residues phosphorylated by TORC1 with Asp/Glu renders Sch9 activity TORC1-independent. Sch9 is required for TORC1 to properly regulate ribosome biogenesis, translation initiation and entry into G0 phase, but not expression of Gln3-dependent genes. Our results suggest that Sch9 functions analogously to the mammalian TORC1 substrate S6K1 rather than the mTORC2 substrate PKB/Akt. Keywords: time course, cell type. Global transcriptional analysis of rapamycin response was conducted on cells expressing either a wild-type, Sch9(WT), or TOR-independent allele of Sch9, Sch9(2D3E). Reference samples used were cells collected immediately prior to rapamycin treatment for the respective cell genotypes. Test samples were collected 20, 30, 60, 90, 120, and 180min post rapamycin treatment.
Project description:Aneuploidy, or an aberrant karyotype, results in developmental disabilities and has been implicated in tumorigenesis. However, the causes of aneuploidy-induced phenotypes and the consequences of aneuploidy on cell physiology remain poorly understood. We have performed a meta-analysis on gene expression data from aneuploid cells in diverse organisms, including yeast, plants, mice, and humans. We found highly-related gene expression patterns that are conserved between species: genes that were involved in the response to stress were consistently upregulated, while genes associated with the cell cycle and cell proliferation were downregulated in aneuploid cells. Within species, different aneuploidies induced similar changes in gene expression, independent of the specific chromosomal aberrations. Taken together, our results demonstrate that aneuploidies of different chromosomes and in different organisms impact similar cellular pathways and cause a stereotypical anti-proliferative response that must be overcome prior to transformation. These experiments are two-color hybridizations of RNA isolated from aneuploid samples vs matched wt cells, all grown to midlog phase.