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Transcriptomic screen to identify genes regulated by dSET2 in Drosophila third-instar larval nervous system

ABSTRACT: Gene expression changes in neurons are primarily thought to occur via activity driven transcription of immediate-early genes (Chen et al., 2016). Little notice is given to how intracellular Ca2+ changes downstream of myriad signaling pathways affects neuronal gene expression. We recently identified a set of genes whose expression requires IP3R/Ca2+ signals in larval neurons (Jayakumar et al., 2018). This work studies how IP3R/Ca2+ signals regulate changes in gene expression, critical to growth and development, through the histone methyltransferase dSET2. In this study we investigate how IP3R and dSET2 regulate a common set of developmentally significant genes to enable the larval to pupal transition on a protein deprived diet.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE162094 | GEO | 2020/11/25

REPOSITORIES: GEO

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Transcriptomic screen to identify genes regulated by IP3R in Drosophila third-instar larval nervous system

Project description:Organisms need to co-ordinate growth with development particularly in the context of nutrient availability. Thus, multiple ways have evolved to survive extrinsic nutrient deprivation during development. In the holometabolous insect Drosophila, growth occurs during larval development. Larvae are therefore critically dependent on nutritional inputs for pupariation. Post critical weight however, they pupariate even when starved. How nutrient availability is coupled to the internal metabolic state for the decision to pupariate in not well understood and needs better understanding. Wild type larvae, when subjected to nutrient deprivation as mid-third instar larvae, pupariate and also emerge as adults, even though smaller than normally fed ones (Jayakumar et al., 2016; Megha and Hasan, 2017). A recent study (Jayakumar et al., 2016) identified a neuronal circuit that enables wild-type larvae to survive protein deprivation and pupariate. IP3R function in a subset of glutamatergic neurons is a crucial part of the circuit. However, the cellular role of IP3R in these neurons is not understood. In Drosophila neurons, the IP3R causes and facilitates store-operated calcium entry (Chakraborty et al., 2016; Venkiteswaran and Hasan, 2009). Thus it is likely, that the IP3R also regulates expression of genes that regulate this phenomenon. In this study, we have compared the gene expression profiles of control and itpr knockdown larval brains to identify genes that act downstream of the IP3R to regulate pupariation under nutrition stress.

2019-03-01 | GSE109637 | GEO

Cytokinesis signals truncation of the PodJ polarity factor by a cell cycle-regulated protease

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Project description:The activation of IP3 receptor (IP3R) Ca2+ channels generates agonist-mediated Ca2+ signals that are critical for the regulation of a wide range of biological processes. It is therefore surprising that CRISPR induced loss of all three IP3R isoforms (TKO) in HEK293 and HeLa cell lines yields cells that can survive, grow and divide, albeit more slowly than wild-type cells. In an effort to understand the adaptive mechanisms involved, we have examined the activity of key Ca2+ dependent transcription factors (NFAT, CREB and AP-1) and signaling pathways using luciferase-reporter assays, phosphoprotein immunoblots and whole genome transcriptomic studies. In addition, the diacylglycerol arm of the signaling pathway was investigated with protein kinase C (PKC) inhibitors and siRNA knockdown. The data showed that agonist-mediated NFAT activation was lost but CREB activation was maintained in IP3R TKO cells. Under base-line conditions transcriptome analysis indicated the differential expression of 828 and 311 genes in IP3R TKO HEK293 or HeLa cells, respectively, with only 18 genes being in common. Three main adaptations in TKO cells were identified in this study: 1) increased basal activity of NFAT, CREB and AP-1; 2) an increased reliance on Ca2+- insensitive PKC isoforms; and 3) increased production of reactive oxygen species and upregulation of antioxidant defense enzymes. We suggest that whereas wild-type cells rely on a Ca2+ and DAG signal to respond to stimuli, the TKO cells utilize the adaptations to allow key signaling pathways (e.g. PKC, Ras/MAPK, CREB) to transition to the activated state using a DAG signal alone.

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KLF4 Time Course

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2011-05-30 | GSE28456 | GEO

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2021-06-21 | GSE166738 | GEO

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2021-12-28 | GSE169371 | GEO

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