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Whole transcriptome analysis identifies differentially regulated networks during the proliferation inhibition and megakaryocytic differentiation of AML cell induced by 3,8-Di-O-methylellagic acid 2-O-glucoside (DMAG) derived from Sanguisorba offcinalis L.

ABSTRACT: We identified the expression profiles of lncRNA, mRNA, miRNA and circRNA by whole-transcriptome sequencing and constructed co-expression network to elucidate the potential mechanisms of 3,8-Di-O-methylellagic acid 2-O-glucoside in anti-AML eﬀect

ORGANISM(S): Homo sapiens

PROVIDER: GSE142994 | GEO | 2022/01/01

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE142994_Annotated_lncRNA_FPKM.txt.gz	Txt
	GSE142994_Novel_lncRNA_FPKM.txt.gz	Txt
	GSE142994_circRNA_Readcount_TPM.txt.gz	Txt
	GSE142994_mRNA_FPKM.txt.gz	Txt

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Whole transcriptome analysis identifies differentially regulated networks during the proliferation inhibition and megakaryocytic differentiation of AML cell induced by 3,8-Di-O-methylellagic acid 2-O-glucoside (DMAG) derived from Sanguisorba offcinalis L.

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Project description:The obligate intracellular bacterium Chlamydia alternates between two functional forms during its developmental cycle: elementary body (EB) and reticulate body (RB). However, the molecular mechanisms governing the transitions between these forms are unknown. Here, we present evidence cyclic di-AMP (c-di-AMP) is a key factor in triggering the transition from RB to EB (i.e., secondary differentiation) in the chlamydial developmental cycle. We made strains producing different levels of c-di-AMP, which we linked to changes in secondary differentiation status. Increases in c-di-AMP resulted in an earlier increase in transcription of EB-associated genes, and this was further manifested in earlier production of EBs. In contrast, when c-di-AMP levels were decreased, secondary differentiation was delayed. Based on these data, we conclude there is a threshold level of c-di-AMP needed to trigger secondary differentiation in Chlamydia. This is the first study to define a mechanism of secondary differentiation in Chlamydia.

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Project description:C-di-AMP is primarily associated with the regulation of carbon utilization as well as other central traits, central metabolism, and bacterial stringent response to environmental changes. Elevated c-di-AMP levels result in aberrant physiology for most c-di-AMP synthesizing organisms, drawing particular attention to the importance of the c-di-AMP homeostasis and the molecular mechanisms pertaining to nucleotide metabolism and signal transduction. Here we show that c-di-AMP binds the GntR-family regulator DasR, uncovering a direct link between c-di-AMP and GlcNAc signaling. Further, we show c-di-AMP functions as an allosteric activator of DasR activity. GlcNAc is necessary for cell-surface structure from bacteria to humans, as well as a signal for bacterial development and antibiotic production. DasR is a global repressor that oversees GlcNAc metabolism and antibiotic production, which enables Actinobacteria to cope with stress and starvation. Our in vivo studies reveal the important biological role of allosteric regulation by c-di-AMP in metabolic imbalance and the transduction of a series of signals. Notably, DasR also controls intracellular c-di-AMP level through direct repression on disA. Overall, we identify a function of allosteric regulation between c-di-AMP and DasR in global signal integration and c-di-AMP homeostasis in bacteria, which is likely widespread in Actinobacteria.

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