Nuclear autophagy: An evolutionarily conserved mechanism of nuclear degradation in the cytoplasm

Luo, Majing; Zhao, Xueya; Song, Ying; Cheng, Hanhua; Zhou, Rongjia

doi:10.1080/15548627.2016.1217381

Cited by 74 publications

(62 citation statements)

References 78 publications

(113 reference statements)

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“…Ferritinophagy, as a recently discovered selective autophagy, is remarkably different from some other selective autophagy, such as mitophagy (Liu et al, ; Novak et al, ; Okamoto, Kondo‐Okamoto, & Ohsumi, ; Quinsay, Thomas, Lee, & Gustafsson, ), reticulophagy (Khaminets et al, ; Mochida et al, ), glycophagy (Jiang, Wells, & Roach, ), xenophagy (Thurston, Wandel, von Muhlinen, Foeglein, & Randow, ), aggrephagy (Liu et al, ; Rogov, Dotsch, Johansen, & Kirkin, ), pexophagy (Farre, Manjithaya, Mathewson, & Subramani, ; Motley, Nuttall, & Hettema, ), nucleophagy (Luo, Zhao, Song, Cheng, & Zhou, ; Mochida et al, ), ribophagy (Kraft, Deplazes, Sohrmann, & Peter, ), DNautophagy (Aizawa et al, ; Fujiwara, Hase, Wada, & Kabuta, ), and RNautophagy (Fujiwara et al, ; Hase et al, ; Table ). Although NCOA4‐mediated ferritinophagy has been certified to be responsible for erythropoiesis via releasing iron, the specific transferred way of ferritinophagy‐derived iron delivering to mitochondria warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

Ferritinophagy/ferroptosis: Iron‐related newcomers in human diseases

Tang

Chen

et al. 2018

Journal Cellular Physiology

211

141

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Nuclear receptor coactivator 4 mediated ferritinophagy is an autophagic phenomenon that specifically involves ferritin to release intracellular free iron. Ferritinophagy is implicated in maintaining efficient erythropoiesis. Notably, ferritinophagy also plays a central role in driving some pathological processes, including Parkinson's disease (PD) and urinary tract infections. Some evidence has demonstrated that ferritinophagy is critical to induce ferroptosis. Ferroptosis is a newly nonapoptotic form of cell death, characterized by the accumulation of iron-based lipid reactive oxygen species. Ferroptosis plays an important role in inhibiting some types of cancers, such as hepatocellular carcinoma, pancreatic carcinoma, prostate cancer, and breast cancer. Conversely, the activation of ferroptosis accelerates neurodegeneration diseases, including PD and Alzheimer's disease. Therefore, in this review, we summarize the regulatory mechanisms related to ferritinophagy and ferroptosis. Moreover, the distinctive effects of ferritinophagy in human erythropoiesis and some pathologies, coupled with the promotive or inhibitory role of tumorous and neurodegenerative diseases mediated by ferroptosis, are elucidated. Obviously, activating or inhibiting ferroptosis could be exploited to achieve desirable therapeutic effects on diverse cancers and neurodegeneration diseases. Interrupting ferritinophagy to control iron level might provide a potentially therapeutic avenue to suppress urinary tract infections.

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Section: Discussionmentioning

confidence: 99%

Ferritinophagy/ferroptosis: Iron‐related newcomers in human diseases

Tang

Chen

et al. 2018

Journal Cellular Physiology

211

141

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“…Recently, new evidence demonstrated that some plant viruses can repress or use autophagy to promote the viral infection Li et al, 2017;Hafr en et al, 2018;Yang et al, 2018;Huang et al, 2019). However, how autophagic substrates in the nucleus are sequestered and transferred into the cytoplasm for autophagic degradation remains unknown (Luo et al, 2016), and whether the nuclear autophagy-mediated degradation of viral proteins operates in plants is not clear either. However, how autophagic substrates in the nucleus are sequestered and transferred into the cytoplasm for autophagic degradation remains unknown (Luo et al, 2016), and whether the nuclear autophagy-mediated degradation of viral proteins operates in plants is not clear either.…”

Section: Discussionmentioning

confidence: 99%

“…To maintain nuclear homeostasis, cells also require a strategy for eliminating undesirable nuclear components in response to stress or pathogen infection (Luo et al, 2016). To maintain nuclear homeostasis, cells also require a strategy for eliminating undesirable nuclear components in response to stress or pathogen infection (Luo et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Nuclear autophagy degrades a geminivirus nuclear protein to restrict viral infection in solanaceous plants

Zhang

et al. 2019

New Phytologist

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Autophagy is an evolutionarily conserved degradation pathway in the cytoplasm and has emerged as a key defense mechanism against invading pathogens. However, there is no evidence showing nuclear autophagy in plants.Here, we show that a geminivirus nuclear protein, C1 of tomato leaf curl Yunnan virus (TLCYnV) induces autophagy and interacts directly with the core autophagy-related protein ATG8h. The interaction between ATG8h and C1 leads to the translocation of the C1 protein from the nucleus to the cytoplasm and the decreased protein accumulation of C1, which is dependent on the exportin1-mediated nuclear export pathway. The degradation of C1 is blocked by autophagy inhibitors and compromised when the autophagy-related genes (ATGs) ATG8h, ATG5, or ATG7 are knocked down. Similarly, silencing of these ATGs also promotes TLCYnV infection in Nicotiana benthamiana and Solanum lycopersicum plants.The mutation of a potential ATG8 interacting motif (AIM) in C1 abolishes its interaction with ATG8h in the cytoplasm but favors its interaction with Fibrillarin1 in the nucleolus. TLCYnV carrying the AIM mutation displays enhanced pathogenicity in solanaceous plants.Taken together, these data suggest that a new type of nuclear autophagy-mediated degradation of viral proteins through an exportin1-dependent nuclear export pathway restricts virus infection in plants.

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“…Although both Trib3 and AKT2 primarily reside in the nucleus, there is a chance that Trib3-AKT2 complex will migrate to cytoplasm, and cytoplasmic E3 ligase stimulates ubiquitination and autophagic degradation of AKT2. Alternatively, Trib3 might recruit E3 ligase to AKT2 in the nucleus, and nuclear autophagy could process ubiquitinated AKT2 [50,51]. Identifying E3 ligase, which promotes AKT2 ubiquitination together with Trib3, and the mechanism of how these processes target AKT2 to autophagosome, perhaps examining the topologies of Trib3-dependent AKT2 polyubiquitination and whether that E3 ligase is associated with insulin resistance is worth considering for future studies.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Tissue Trib3 Links Obesity with Insulin Resistance by Autophagic Degradation of AKT2

Kwon

Eom

Kim

et al. 2018

Cell Physiol Biochem

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Background/Aims: Obesity is a serious health risk factor strongly associated with insulin resistance and type 2 diabetes; however, the underlying mechanisms associating obesity with insulin resistance remain unknown. In this study, we explored the physiological role of Trib3 in regulating glucose metabolism in skeletal muscle tissues in a Trib3 transgenic mice model. Methods: Glucose metabolism in transgenic mice overexpressing Trib3 specifically in the skeletal muscle was examined by glucose/insulin tolerance test, metabolic cage studies, and glucose uptake assay. The effect of Trib3 overexpression on AKT phosphorylation and AKT protein turnover were assessed by RT-PCR and immunoblot analysis. Subcellular distribution of Trib3 and AKT1/2 was determined by microscopic analysis, co-immunoprecipitation experiments, and limited-detergent extraction of subcellular organelles. Ubiquitin assay was performed and ATG7 deficient cell line was employed to address the mechanisms of Trib3-dependent AKT protein homeostasis. Results: We found that Trib3 expression in skeletal muscle is elevated in obese conditions, and transgenic mice that overexpressed Trib3, specifically in skeletal muscle tissues, displayed impaired glucose homeostasis by suppressing insulin-stimulated glucose uptake. Disruption of insulin signaling in skeletal muscle Trib3 transgenic mice may occur due to the specific downregulation of AKT2 but not AKT1. Autophagy regulated AKT2 protein turnover, and Trib3 overexpression stimulated autophagic degradation of AKT2 by promoting AKT2 ubiquitination. Conclusion: Because diet-induced obesity upregulates Trib3 and downregulates AKT2 in skeletal muscle tissues, Trib3 may play a key role in establishing an association between obesity and insulin resistance by regulating AKT2 protein homeostasis.

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Nuclear autophagy: An evolutionarily conserved mechanism of nuclear degradation in the cytoplasm

Cited by 74 publications

References 78 publications

Ferritinophagy/ferroptosis: Iron‐related newcomers in human diseases

Ferritinophagy/ferroptosis: Iron‐related newcomers in human diseases

Nuclear autophagy degrades a geminivirus nuclear protein to restrict viral infection in solanaceous plants

Skeletal Muscle Tissue Trib3 Links Obesity with Insulin Resistance by Autophagic Degradation of AKT2

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