Protein disulfide isomerase PDI-6 regulates Wnt secretion to coordinate inter-tissue UPRmt activation and lifespan extension in C. elegans

Li, Xinyu; Li, Jiasheng; Zhu, Di; Zhang, Ning; Hao, Xusheng; Zhang, Wenfeng; Zhang, Qian; Liu, Yangli; Wu, Xueying; Tian, Ye

doi:10.1016/j.celrep.2022.110931

Cited by 14 publications

(7 citation statements)

References 78 publications

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“…Moreover, the longest-lived rodent (the naked mole-rat) is characterized by an above-average number of chaperones and shows the distinct ability to maintain proteostasis via proteasomemediated degradation and autophagy during aging (Draceni and Pechmann, 2019;Rodriguez et al, 2016). In addition, the UPR ER rate is decreased in aged C. elegans (Ben-Zvi et al, 2009), whereas an increased UPR mito rate extends worm lifespan (Li et al, 2022g). All these results suggest that chaperone status, the activities of the autophagy-lysosomal system, the ubiquitin-proteasome system, and the functionality of UPR ER and UPR mito can be used as biomarkers of aging.…”

Section: Loss Of Proteostasismentioning

confidence: 99%

Biomarkers of aging

Bao

Cao

Chen

et al. 2023

Sci. China Life Sci.

124

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Aging biomarkers are a combination of biological parameters to (i) assess age-related changes, (ii) track the physiological aging process, and (iii) predict the transition into a pathological status. Although a broad spectrum of aging biomarkers has been developed, their potential uses and limitations remain poorly characterized. An immediate goal of biomarkers is to help us answer the following three fundamental questions in aging research: How old are we? Why do we get old? And how can we age slower? This review aims to address this need. Here, we summarize our current knowledge of biomarkers developed for cellular, organ, and organismal levels of aging, comprising six pillars: physiological characteristics, medical imaging, histological features, cellular alterations, molecular changes, and secretory factors. To fulfill all these requisites, we propose that aging biomarkers should qualify for being specific, systemic, and clinically relevant. Supporting Information The supporting information is available online at 10.1007/s11427-023-2305-0. The supporting materials are published as submitted, without typesetting or editing. The responsibility for scientific accuracy and content remains entirely with the authors.

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Section: Loss Of Proteostasismentioning

confidence: 99%

Biomarkers of aging

Bao

Cao

Chen

et al. 2023

Sci. China Life Sci.

124

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“…The oxidative stress-mediated balance of the FOXO/Wnt signaling axis plays an important role in maintaining the homeostasis of the intracellular environment ( Bourgeois et al, 2021 ). Knockdown or mutation of different Wnt ligands in C. elegans can affect worm lifespan, indicating that changes in the Wnt microenvironment can also directly affect senescence ( Li et al, 2022 ). mTOR is one of the major intracellular targets of IIS (insulin/IGF-1 signaling), which is triggered in response to adequate nutrient supply and growth factor signals.…”

Section: Resultsmentioning

confidence: 99%

Curcumin supplementation increases longevity and antioxidant capacity in Caenorhabditis elegans

Liu

et al. 2023

Front. Pharmacol.

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Curcumin is well known as a potent antioxidant and free radical scavenger and has great potential for anti-aging applications. In this study, we investigate the molecular mechanism of curcumin in prolonging the lifespan of C. elegans. Four concentrations of curcumin (10, 25, 50, and 100 µM) were administered, and the optimal treatment concentration was determined by analyzing the nematode lifespan, physiology, and biochemistry. Additionally, RNA-seq and qRT-PCR were performed to explore the antioxidant effect of curcumin and its underlying mechanism. Results revealed that curcumin could significantly improve the survival capacity of C. elegans without influencing its growth. Curcumin was observed to significantly decrease the levels of reactive oxygen species (ROS) under extreme conditions such as heat stress and paraquat stress. In addition, curcumin increased the amount of nematode mitochondrial DNA (mtDNA) replication. RNA-seq results revealed that the underlying mechanism of curcumin in C. elegans is related to the mitogen-activated protein kinase (MAPK) pathway. qRT-PCR results confirmed that the expression of oxidative stress-related genes (sod-1, sod-2, sod-3, gst-4) was increased, and the expression of MAPK signaling pathway-related genes (sek-1, pmk-1, nsy-1) was significantly downregulated. Furthermore, the administration of curcumin extended the lifespan of nematodes, potentially through the enhancement of oxidative stress resistance and the downregulation of the MAPK signaling pathway. These findings improve our understanding of both lifespan extension and the potential mechanism of curcumin in C. elegans.

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“…PRV has been used as a model virus for studying the molecular biology of the human herpesvirus HSV-1 8 . The UL23 protein is a thymidine kinase 9 that catalyzes the synthesis of viral DNA, participates in virus replication, and the spread of the virus in the central nervous system 10 . It has been reported that PRV lacking thymidine kinase UL23 exhibits significantly reduced virulence in infected swine 11 .…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal regulation of Pseudorabies Virus Thymidine kinase UL23 by post-translational modification

Li,

Cao,

Zhang

et al. 2024

Preprint

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Post-translational modification plays a significant role in the interaction between viruses and their hosts. The pseudorabies virus (PRV) is a highly contagious herpesvirus that affects the central nervous system and respiratory tract of swine. However, the role of post-translational modifications, including Ubiquitination and SUMOylation, in host and PRV interplays is poorly understood. Here we examined the SUMO modification of PRV proteins and revealed that the PRV thymidine kinase UL23 can undergo SUMO modification. Bioinformatic analysis suggested four potential modification sites for UL23. Site-directed mutagenesis indicates that SUMO modification occurs at sites K242 and K267 as the wild type localizes in the nucleus while the mutants localize in the cytoplasm. Subsequently, polyclonal antibodies against mouse derived UL23 were employed to reveal that wild type UL23 was mainly located in the nucleus during PRV infection. Co-expression of UL23 with SUMO deconjugating enzymes showed that SENP1/2 inhibited the nuclear import of UL23. Whereas SUMO modification significantly impacted the localization of UL23, it did not detectably affect its stability.

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Protein disulfide isomerase PDI-6 regulates Wnt secretion to coordinate inter-tissue UPRmt activation and lifespan extension in C. elegans

Cited by 14 publications

References 78 publications

Biomarkers of aging

Biomarkers of aging

Curcumin supplementation increases longevity and antioxidant capacity in Caenorhabditis elegans

Spatiotemporal regulation of Pseudorabies Virus Thymidine kinase UL23 by post-translational modification

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