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Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE254193 | GEO | 2024/10/28

REPOSITORIES: GEO

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Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [YY1 CUT&RUN]

Project description:Neurons deploy diverse adaptive strategies to ensure survival and neurotransmission amid cellular stress. Yet, when these adaptive pathways are overwhelmed, functional impairment or neurodegeneration follow. Herein we report a scenario where stressed neurons actively adopt a state of transmissive dormancy, despite rapid activation of stress response pathways, as a terminal protective measure. Examination of dopaminergic neurons surviving severe cellular stress, revealed decreased spontaneous activity accompanied by dynamic control of dopamine metabolism through the Yin Yang 1 (YY1) transcriptional regulator. Under conditions of ionic imbalance or oxidative stress, YY1 promotes expression of the SLC18A2 transporter with the capacity to enhance sequestration of dopamine into transport vesicles. Subsequent DNA damage represses the rate-limiting enzyme in dopamine synthesis, tyrosine hydroxylase (TH), through YY1 mediated stabilization of an intronic guanine quadruplex. This cascade has the potential to drive circuit inactivation and safeguard neurons by minimizing the toxic accumulation of cytosolic dopamine and reducing the energetic expenditure associated with cellular depolarization. In essence, neurons appear to actively prioritize viability over functionality.

2024-10-28 | GSE254192 | GEO

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [BG4 CUT&RUN]

Project description:Neurons deploy diverse adaptive strategies to ensure survival and neurotransmission amid cellular stress. When these adaptive pathways are overwhelmed, functional impairment or neurodegeneration follows. Here, we report a scenario where stressed neurons actively induce a state of transmissive dormancy as a protective measure. Examination of dopaminergic neurons surviving severe cellular challenges revealed decreased spontaneous activity accompanied by dynamic control of dopamine metabolism through the transcriptional regulator Yin Yang 1 (YY1). Under these conditions, YY1 increases expression of the vesicular monoamine transporter 2, promoting sequestration of dopamine into synaptic vesicles. Following oxidative stress and subsequent DNA damage, YY1 inhibits dopamine synthesis through stabilization of a guanine quadruplex in intron 10 of tyrosine hydroxylase. This cytoprotective response has the potential to drive circuit inactivation and safeguard neurons by minimizing the toxic accumulation of cytosolic dopamine and inducing a state of neuronal dormancy. In essence, neurons appear to actively prioritize viability over functionality.

2024-10-28 | GSE275940 | GEO

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [TG timeline RNA-seq]

2024-10-28 | GSE254139 | GEO

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy

Project description:Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy

| PRJNA1068969 | ENA

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [YY1 CUT&RUN]

Project description:Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [YY1 CUT&RUN]

| PRJNA1068976 | ENA

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [BG4 CUT&RUN]

Project description:Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [BG4 CUT&RUN]

| PRJNA1153920 | ENA

Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [TG timeline RNA-seq]

Project description:Yin Yang 1 and guanine quadruplexes protect dopaminergic neurons from cellular stress via transmissive dormancy [TG timeline RNA-seq]

| PRJNA1068619 | ENA

The yin-yang of KIR3DL1/S1: molecular mechanisms and cellular function.

Project description:Killer Immunoglobulin-like Receptors (KIR) are a family of receptors expressed on natural killer (NK) and T-cell subsets. KIR3DL1 is a highly polymorphic receptor that binds to groups of HLAA and HLA-B allotypes that express the Bw4 epitope. The variation in KIR3DL1 allotypes manifests at a number of levels. Most dramatically, a common allelic variant encodes an activating rather than an inhibitory receptor (KIR3DS1). In addition, sequence variants can affect both the frequency of expression within the NK cell population and the intensity of expression on a given cell. KIR3DL1 polymorphism also influences the interaction with HLA-Bw4 molecules, due to contacts with the HLA molecule itself and sensitivity to the presented peptide. A body of evidence from genetic association studies supports the biological significance not only of the interaction of KIR3DL1 with HLA-Bw4 but also the functional variation seen with different KIR3DL1 and HLA allotypes. In this review, we discuss our current understanding of KIR3DL1 function and our recent insights from the structure of the KIR3DL1 in complex with HLA. In addition, we will summarize our current understanding of KIR3DS1, including its ligand specificity and its role in immune responses.

| S-EPMC3741655 | biostudies-literature

Antioxidants protect PINK1-dependent dopaminergic neurons in Drosophila.

Project description:Parkinson's disease (PD) is the most frequent neurodegenerative movement disorder. Mutations in the PINK1 gene are linked to the autosomal recessive early onset familial form of PD. The physiological function of PINK1 and pathological abnormality of PD-associated PINK1 mutants are largely unknown. We here show that inactivation of Drosophila PINK1 (dPINK1) using RNAi results in progressive loss of dopaminergic neurons and in ommatidial degeneration of the compound eye, which is rescued by expression of human PINK1 (hPINK1). Expression of human SOD1 suppresses neurodegeneration induced by dPINK1 inactivation. Moreover, treatment of dPINK1 RNAi flies with the antioxidants SOD and vitamin E significantly inhibits ommatidial degeneration. Thus, dPINK1 plays an essential role in maintaining neuronal survival by preventing neurons from undergoing oxidative stress, thereby suggesting a potential mechanism by which a reduction in PINK1 function leads to PD-associated neurodegeneration.

| S-EPMC1569195 | biostudies-literature

A possible representation of Yin Yang five elements (Yin Yang Wu Xing): Hypothesis of Dual Five-Body-Coordination.

Project description:BackgroundThe idea of Yin Yang Wu Xing, traditionally adopted and practiced in East-Asian medicine, has not been incorporated into the theoretical framework of modern medicine. It is therefore desired to show that Yin Yang Wu Xing is a manifestation of a higher-level faculty of cooperating system, thus making it suitable for a modern frame of thought.MethodsA higher-level faculty of the cooperating system is formulated in the scheme of Dual Five-Body Coordination. The stability of this scheme is examined mathematically and the feasibility of its physical realization is estimated.ResultsThe Dual Five-Body Coordination scheme, which overlaps substantially with the conceptual structure of Yin Yang Wu Xing, is stable and has survival merit. An imaginable conjecture based on physical reality confirms its physical feasibility.ConclusionThe Dual Five-Body Coordination scheme has potential utilization in various fields including biology and sociology. Once the theoretical framework is solidified, the Dual Five-Body Coordination scheme can be readily applied in practical research in modern medicine.

| S-EPMC7473878 | biostudies-literature

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