The TORC1 signaling pathway regulates respiration-induced mitophagy in yeast

Liu, Yang; Okamoto, Koji

doi:10.1016/j.bbrc.2018.05.123

Cited by 15 publications

(7 citation statements)

References 31 publications

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“…In addition, we also observed a reduction in the expression of GTR1, which is an activator TORC1. GTR1 was shown to be negatively regulated upon nutrient starvation [82], and its deletion led to reduced activity of TORC1 [83]. In line with the established relationship between the TORC1-Sch9 pathway and Rim15 protein kinase, we observed the upregulated expression of the RIM15 gene.…”

Section: Discussionsupporting

confidence: 79%

Antiaging Effect of 4-N-Furfurylcytosine in Yeast Model Manifests through Enhancement of Mitochondrial Activity and ROS Reduction

2022

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Small compounds are a large group of chemicals characterized by various biological properties. Some of them also have antiaging potential, which is mainly attributed to their antioxidant activity. In this study, we examined the antiaging effect of 4-N-Furfurylcytosine (FC), a cytosine derivative belonging to a group of small compounds, on budding yeast Saccharomyces cerevisiae. We chose this yeast model as it is known to contain multiple conserved genes and mechanisms identical to that of humans and has been proven to be successful in aging research. The chronological lifespan assay performed in the study revealed that FC improved the viability of yeast cells in a concentration-dependent manner. Furthermore, enhanced mitochondrial activity, together with reduced intracellular ROS level, was observed in FC-treated yeast cells. The gene expression analysis confirmed that FC treatment resulted in the restriction of the TORC1 signaling pathway. These results indicate that FC has antiaging properties.

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Section: Discussionsupporting

confidence: 79%

Antiaging Effect of 4-N-Furfurylcytosine in Yeast Model Manifests through Enhancement of Mitochondrial Activity and ROS Reduction

2022

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“…Rapamycin is another inhibitor of mTOR, which is the most commonly used as an inducer of autophagy, but we should notice that it can affect both mTORC1 and mTORC2. What's more, mTOR is a major regulatory protein that is part of several signaling pathways, including for example those that respond to INS/insulin, EGF/epidermal growth factor and amino acids, and it thus controls process other than autophagy 54-57. Therefore, rapamycin will ultimately affect many metabolic pathways and the pleiotropic effects need to be considered 58.…”

Section: Regulatory Mechanism Of Autophagy In Endometriummentioning

confidence: 99%

Role of Endometrial Autophagy in Physiological and Pathophysiological Processes

Yang

Wang

et al. 2019

J. Cancer

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Endometrium is the mucosal lining of the uterus which expressed a cyclic process of proliferation, secretion and scaling under the control of hormones secreted by the ovary, and it also plays an indispensable role in the embryo implantation, the constitution of fetal-maternal interface, and the maintaining of pregnancy. In pathophysiological conditions, the abnormality or disorder of endometrium may lead to endometrium-related diseases, such as endometriosis, endometrium hyperplasia and even endometrial carcinoma. In recent years, more and more evidence revealed that autophagy exists in both the endometrium stroma cells and epithelial cells, and the activity of autophagy is changed in the different phases of menstruation, as well as in the endometrium-related diseases. Here, we aim to review the activity level, the regulatory factors and the function of autophagy in physiological and pathophysiological endometria, and to discuss the potential value of autophagy as a target for therapies of endometrium-related diseases.

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“…Moreover, excess activation of TORC1 (Tor complex Ⅰ) seems to destabilize Atg32-Atg11 interactions [42]. Loss of Npr2, a component of the SEACIT (Seh1-associated complex inhibiting TORC1) complex that suppresses TORC1 activity, significantly reduces mitophagy during prolonged respiration.…”

Section: Phosphorylation Of Atg32mentioning

confidence: 99%

Mitochondrial clearance: mechanisms and roles in cellular fitness

Onishi

Okamoto

2021

FEBS Letters

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Edited by Agnieszka ChacinskaMitophagy is one of the selective autophagy pathways that catabolizes dysfunctional or superfluous mitochondria. Under mitophagy-inducing conditions, mitochondria are labeled with specific molecular landmarks that recruit the autophagy machinery to the surface of mitochondria, enclosed into autophagosomes, and delivered to lysosomes (vacuoles in yeast) for degradation. As damaged mitochondria are the major sources of reactive oxygen species, mitophagy is critical for mitochondrial quality control and cellular health. Moreover, appropriate control of mitochondrial quantity via mitophagy is vital for the energy supply-demand balance in cells and whole organisms, cell differentiation, and developmental programs. Thus, it seems conceivable that defects in mitophagy could elicit pleiotropic pathologies such as excess inflammation, tissue injury, neurodegeneration, and aging. In this review, we will focus on the molecular basis and physiological relevance of mitophagy, and potential of mitophagy as a therapeutic target to overcome such disorders.

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The TORC1 signaling pathway regulates respiration-induced mitophagy in yeast

Cited by 15 publications

References 31 publications

Antiaging Effect of 4-N-Furfurylcytosine in Yeast Model Manifests through Enhancement of Mitochondrial Activity and ROS Reduction

Antiaging Effect of 4-N-Furfurylcytosine in Yeast Model Manifests through Enhancement of Mitochondrial Activity and ROS Reduction

Role of Endometrial Autophagy in Physiological and Pathophysiological Processes

Mitochondrial clearance: mechanisms and roles in cellular fitness

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