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Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells [ChIP-Seq]

ABSTRACT: Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells [ChIP-Seq]

PROVIDER: PRJNA547601 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9211782_1.fastq.gz	Fastqsanger.gz
	SRR9211782_2.fastq.gz	Fastqsanger.gz
	SRR9211783.fastq.gz	Fastqsanger.gz

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Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells

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Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells [ChIP-Seq]

Project description:Translation is a basic cellular process and its capacity is adapted to cell function. In particular, secretory cells achieve high protein synthesis levels without triggering the protein stress response. It is unknown how and when translation capacity is increased during differentiation. Here, we show that the transcription factor Creb3l2 is a scaling factor for translation capacity in pituitary secretory cells and that it directly binds ~75% of regulatory and effector genes for translation. In parallel with this cell-autonomous mechanism, implementation of the physiological UPR pathway prevents triggering the protein stress response. The pituitary differentiation factor Tpit activates Creb3l2 expression, the Creb3l2-dependent regulatory network as well as the physiological UPR pathway. Thus, Creb3l2 implements high basal translation levels through direct targeting of translation effector genes acting downstream of signaling pathways that otherwise regulate protein synthesis. Expression of Creb3l2 may be a useful means to enhance production of therapeutic proteins.

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Cell-autonomous transcriptional mechanism for enhancement of translation capacity in secretory cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Autonomous circadian bladder capacity rhythm independent of the central clock

Project description:This study investigates the autonomous regulatory function of the bladder for its capacity circadian rhythm using a central nervous Bmal1 conditional knockout (cKO) mouse. Under constant darkness (DD), these mice lose behavioral rhythmicity but preserve rhythmicity of the bladder capacity and bladder clock gene expression for short term. However, prolonged exposure to DD results in loss of bladder capacity rhythm and decreased clock gene amplitude. RNA-seq analysis in the bladder of Bmal1 cKO mice revealed that clock genes and extracellular matrix-related genes were disrupted in rhythmicity under long DD. These findings highlight that the bladder has an autonomous regulatory function for the diurnal rhythm of bladder capacity independent of the central clock. However, the vulnerability of peripheral bladder clocks is revealed in the long-term absence of central clock input. This study provides molecular insights into how circadian dysregulation may contribute to bladder dysfunction.

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Autonomous biogenesis of all thirty proteins of the E. coli translation machineryk

Project description:The cell-free biogenesis of the protein translation machinery is essential for the creation of a self-regenerating synthetic cell. Here, we demonstrate the autonomous and simultaneous biogenesis of all thirty proteins of the translation machinery of E. coli in a reconstituted transcription-translation system. We first established self-regeneration of every translation protein by determining the threshold concentration required for its own synthesis from a synthetic gene coding for the protein, thereby demonstrating the functionality of all nascent proteins, separately. Simultaneous biogenesis of multiple translation proteins at their threshold resulted in delayed synthesis below detection levels. To achieve self-regeneration of multiple translation proteins, we induced boundary-free compartmentalization of the reaction by immobilizing the genes on a surface at high density. The co-localization of genes, molecular machinery, messenger RNA and nascent proteins at the surface created sufficient conditions to catalyze the simultaneous self-regeneration of sub-groups up to all thirty translation proteins, as measured by total internal reflection fluorescence on the surface. Our approach provides mechanistic insight and presents a general methodology for the biogenesis of cellular machines toward autonomous synthetic systems.

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