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Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

ABSTRACT: Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

PROVIDER: PRJNA684145 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13238576_1.fastq.gz	Fastqsanger.gz
	SRR13238576_2.fastq.gz	Fastqsanger.gz
	SRR13238577_1.fastq.gz	Fastqsanger.gz
	SRR13238577_2.fastq.gz	Fastqsanger.gz
	SRR13238578_1.fastq.gz	Fastqsanger.gz

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Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

Project description:Phosphatidylethanolamine made in mitochondria has long been recognized as an important precursor for phosphatidylcholine production that occurs in the endoplasmic reticulum (ER). Recently, the strict mitochondrial localization of the enzyme that makes PE in the mitochondrion, phosphatidylserine decarboxylase 1 (Psd1), was questioned. Since a dual localization of Psd1 to the ER would have far-reaching implications, we initiated our study to independently re-assess the subcellular distribution of Psd1. Our results support the unavoidable conclusion that the vast majority, if not all, of functional Psd1 resides in the mitochondrion. Through our efforts, we discovered that mutant forms of Psd1 that impair a self-processing step needed for it to become functional are dually localized to the ER when expressed in a PE-limiting environment. We conclude that severely impaired cellular PE metabolism provokes an ER-assisted adaptive response that is capable of identifying and resolving nonfunctional mitochondrial precursors.

2020-12-11 | GSE162987 | GEO

Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

Project description:For decades, the endoplasmic reticulum (ER)-resident tri-methylation pathway of phosphatidylcholine production that is fed by phosphatidylethanolamine (PE) made in the mitochondrion, served as a phospholipid trafficking paradigm. Recently, the strict mitochondrial localization of the enzyme that makes PE in the mitochondrion, phosphatidylserine decarboxylase 1 (Psd1), was questioned. Since a dual localization of Psd1 to the ER would have far-reaching implications, we initiated our study to independently re-assess the subcellular distribution of Psd1. Our results support the unavoidable conclusion that the vast majority, if not all, of functional Psd1 resides in the mitochondrion. Through our efforts, we discovered that mutant forms of Psd1 that impair a self-processing step needed for it to become functional, are dually localized to the ER when expressed in a PE-limiting environment. We conclude that severely impaired cellular PE metabolism provokes an ER-assisted adaptive response that is capable of identifying and resolving nonfunctional mitochondrial precursors.

2020-12-04 | MSV000086558 | MassIVE

Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors.

Project description:Phosphatidylethanolamine (PE) made in mitochondria has long been recognized as an important precursor for phosphatidylcholine production that occurs in the endoplasmic reticulum (ER). Recently, the strict mitochondrial localization of the enzyme that makes PE in the mitochondrion, phosphatidylserine decarboxylase 1 (Psd1), was questioned. Since a dual localization of Psd1 to the ER would have far-reaching implications, we initiated our study to independently re-assess the subcellular distribution of Psd1. Our results support the unavoidable conclusion that the vast majority, if not all, of functional Psd1 resides in the mitochondrion. Through our efforts, we discovered that mutant forms of Psd1 that impair a self-processing step needed for it to become functional are dually localized to the ER when expressed in a PE-limiting environment. We conclude that severely impaired cellular PE metabolism provokes an ER-assisted adaptive response that is capable of identifying and resolving nonfunctional mitochondrial precursors.

| S-EPMC7921845 | biostudies-literature

GNPS - Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

2020-12-04 | MSV000086558 | GNPS

SAGE detects microRNA precursors.

Project description:BackgroundMicroRNAs (miRNAs) have been shown to play important roles in regulating gene expression. Since miRNAs are often evolutionarily conserved and their precursors can be folded into stem-loop hairpins, many miRNAs have been predicted. Yet experimental confirmation is difficult since miRNA expression is often specific to particular tissues and developmental stages.ResultsAnalysis of 29 human and 230 mouse longSAGE libraries revealed the expression of 22 known and 10 predicted mammalian miRNAs. Most were detected in embryonic tissues. Four SAGE tags detected in human embryonic stem cells specifically match a cluster of four human miRNAs (mir-302a, b, c&d) known to be expressed in embryonic stem cells. LongSAGE data also suggest the existence of a mouse homolog of human and rat mir-493.ConclusionThe observation that some orphan longSAGE tags uniquely match miRNA precursors provides information about the expression of some known and predicted miRNAs.

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Metabolic control of Tfh and humoral immunity by phosphatidylethanolamine

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Hi-C detects novel rearrangements in HL60 and HL60/S4 cell lines

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McKay reversible p53 response

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Tafazzin Regulates Cell State by Modulating Phosphatidylethanolamine and Phosphatidylserine levels

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Evaluation of a New Blood-based Test to Detect Colorectal Cancer and Its Precursors

Project description:The CELTiC panel is a potential blood-based test for detecting colorectal cancer (CRC) and precursors of CRC. This can be useful for CRC screening, since this requires tests that detect cancer in an early stage to maximize the chances of successful treatment. CELTiC combines four markers that can be detected in blood. These markers are composed of so-called messenger RNA (mRNA) and can be viewed as the instructions of our genes to the cell to make certain proteins. Cancer is the result of mutation in these genes. Thus, the mRNA in cancer patients is, depending on the type of mRNA, often abnormal. In earlier studies, the developers of CELTiC found four mRNA’s that are different in patients with CRC compared to healthy individuals. However, CELTiC has not yet been extensively studied in individuals for whom the test is intended: a population undergoing CRC screening. The current study aims to fill this gap. We will assess the ability of CELTiC to detect CRC and precursors of CRC in a population of individuals between 50 and 75 years old in the Netherlands and Italy. This population has already been preselected by having a positive fecal immunochemical test (FIT), a test that is frequently used in CRC screening. This population will undergo a colonoscopy, a procedure where a doctor enters the large bowel through the anus using a flexible camara to assess whether the patient has cancer. Prior to this colonoscopy, we will collect blood samples from the individuals to assess their CELTiC score. After the colonoscopy and the blood analysis, we can assess whether the test adequately detects CRC and precursors of CRC in this population.

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