Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA293523 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2182440.fastq.gz | Fastqsanger.gz | |||
| SRR2182450.fastq.gz | Fastqsanger.gz | |||
| SRR2182460.fastq.gz | Fastqsanger.gz | |||
| SRR2182441.fastq.gz | Fastqsanger.gz | |||
| SRR2182451.fastq.gz | Fastqsanger.gz |
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Project description:In the chronobiology field, a fundamental dichotomy exists to explain daily rhythmicity of biological processes: these can be elicited in response to cyclic extrinsic/environmental signals such as light, or driven endogenously by the circadian clock. In mammals, the circadian clock ticks in almost every cell of the body, and functions based on a network of transcription-translation feedback loops. The PI3K-AKT signaling pathway relays environmental information of nutritional/metabolic state to regulate cell size and proliferation. AKT, a Serine/Threonine protein kinase, is activated by phosphorylation, where phospho-serine 473 (pAKT) serves as a hallmark for its activation. Following activation, it proceeds to phosphorylate dozens of target proteins that convey the signal to regulate gene expression and other key cellular functions. Overall, this pathway is widely known to be activated in response to feeding related signals, and previous studies in mice found elevated pAKT levels in correspondence with food ingestion. However, it is still unknown whether this can (also) be driven through intrinsic mechanisms, such as the circadian clock. Here, we inspected daily activation of AKT both in cultured cells and animal models. Unexpectedly, we found, that neither environmental cues nor the circadian clock were necessary for pAKT rhythms, which exhibited ultradian, rather than circadian, cycles of phosphorylation. In addition, hepatic gene expression also exhibited short rhythms in clock disrupted mice, corresponding with AKT related genes/functions. Reciprocally, inhibition of AKT phosphorylation did not affect the rhythmicity of the circadian clock. Overall, our findings uncover temporal regulation of AKT activation and reveal ultradian molecular rhythmicity that cycles independently of the canonical circadian clock.
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Project description:The 4D organization of the interphase nucleus, or the 4D Nucleome (4DN), reflects a dynamical interaction between 3D genome structure and function and its relationship to phenotype. We present initial analyses of the human 4DN, capturing genome-wide structure using chromosome conformation capture and 3D imaging, and function using RNA-sequencing. We introduce a quantitative index that measures underlying topological stability of a genomic region. Our results show that structural features of genomic regions correlate with function with surprising persistence over time. Furthermore, constructing genome-wide gene-level contact maps aided in identifying gene pairs with high potential for coregulation and colocalization in a manner consistent with expression via transcription factories. We additionally use 2D phase planes to visualize patterns in 4DN data. Finally, we evaluated gene pairs within a circadian gene module using 3D imaging, and found periodicity in the movement of clock circadian regulator and period circadian clock 2 relative to each other that followed a circadian rhythm and entrained with their expression.
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Project description:The circadian clock drives daily changes of physiology, including sleep-wake cycles, by regulating transcription, protein abundance and function. Circadian phosphorylation controls cellular processes in peripheral organs, but little is known about its role in brain function and synaptic activity. We applied advanced quantitative phosphoproteomics to mouse forebrain synaptoneurosomes isolated across 24h, accurately quantifying almost 8,000 phosphopeptides. Remarkably, half of the synaptic phosphoproteins, including numerous kinases, had large-amplitude rhythms peaking at rest-activity and activity-rest transitions. Bioinformatic analyses revealed global temporal control of synaptic function via phosphorylation, including synaptic transmission, cytoskeleton reorganization and excitatory/inhibitory balance. Remarkably, sleep deprivation abolished 98% of all phosphorylation cycles in synaptoneurosomes, indicating that sleep-wake cycles rather than circadian signals are main drivers of synaptic phosphorylation, responding to both sleep and wake pressures.
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Project description:Biological processes are usually associated with genome-wide remodeling of transcription driven by transcription factors (TFs). Identifying key TFs and their spatiotemporal binding patterns are indispensable to understanding how dynamic processes are programmed. We present a computational method, dynamic motif occupancy (DynaMO), which exploits random forest modeling and clustering based enrichment analysis. DynaMO exploits TF motifs and dynamic ChIP-seq data of chromatin surrogates such as histone modifications to infer important TFs and their spatiotemporal binding in biological processes. Application of DynaMO to the yeast ultradian cycle, mouse circadian clock and human neural differentiation exhibits its accuracy and versatility. We further demonstrate the function of stress response regulators Msn2 and Msn4 as key TFs activating yeast glycolysis genes. Msn2/4 regulates the cellular transition from quiescence to growth by accumulating the intracellular acetyl-CoA level through glycolysis. We anticipate DynaMO will be generally useful for elucidating transcriptional programs in dynamic processes.
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Project description:The circadian clock system coordinates metabolic, physiological, and behavioral functions across a 24-hour cycle, crucial for adapting to environmental changes. Disruptions in circadian rhythms contribute to major metabolic pathologies like obesity and Type 2 diabetes. Understanding the regulatory mechanisms governing circadian control is vital for identifying therapeutic targets. It is well characterized that chromatin remodeling at distal enhancer elements shapes the genome topology, supporting rhythmic transcriptional cycles; yet the impact of rhythmic chromatin topology and circadian enhancers in disease states is largely unexplored. In his study, we use 4C-seq techniques in mouse liver to explore how the spatial configuration of the genome adapts to diet, rewiring circadian transcription and contributing to dysfunctional metabolism. We describe daily fluctuations in chromatin contacts between distal regulatory elements of metabolic control genes in livers from lean and obese mice and identify specific lipid-responsive regions recruiting the clock molecular machinery. Our findings highlight the intricate coupling of circadian gene expression to a dynamic nuclear environment under high-fat feeding, supporting a temporally regulated program of gene expression and transcriptional adaptation to diet.
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