Induction of Liver Steatosis in BAP31-Deficient Mice Burdened with Tunicamycin-Induced Endoplasmic Reticulum Stress

Wu, Zhenhua; Yang, Fan; Jiang, Shan; Sun, Xiaoyu; Xu, Jialin

doi:10.3390/ijms19082291

Cited by 23 publications

(23 citation statements)

References 41 publications

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“…Another study with these mice reported the same effects upon tunicamycin treatment, as well as increased levels of ER-stress markers [175]. In Bap31-deficient mice, although not statistically significant, a trend toward increased p-eIF2a, ATF4, and CHOP signaling was observed [175]. Moreover, hepatocytes of these mice show increased lipogenic gene expression and SREBP1C expression, and activation of SREBP signaling.…”

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 75%

“…Bap31-deficient mice show enhanced body weight, increased food intake, and greater liver steatosis after exposure to a HFD [174]. Another study with these mice reported the same effects upon tunicamycin treatment, as well as increased levels of ER-stress markers [175]. In Bap31-deficient mice, although not statistically significant, a trend toward increased p-eIF2a, ATF4, and CHOP signaling was observed [175].…”

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 99%

“…A shared feature of the absence of MFN2, GRP75, BAP31, or CYPD is the activation of UPR [97,156,166,173,175,176]. ER stress was initially proposed as a mechanism that drives insulin resistance-related diseases [177], and altered reticulum proteostasis alteration has also been in the spotlight as a possible driver of metabolic diseases [178].…”

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 99%

“…ER stress provokes hyperactivation of JNK, which phosphorylates and inhibits the insulin receptor IRS1 [177]. MFN2, BAP31, and CYPD ablation provoke an increase in activated JNK [156, 175,176]; however, there (A) GRP75, MFN2, BAP31, or CypD depletion leads to deficient insulin signaling and glucose intolerance. The lack of GRP75, MFN2, BAP31, or CypD at mitochondria-ER contact sites causes deficient insulin signaling and glucose intolerance, probably through a mechanism that involves ER UPR or mt UPR.…”

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 99%

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Metabolic implications of organelle–mitochondria communication

2019

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Cellular organelles are not static but show dynamism—a property that is likely relevant for their function. In addition, they interact with other organelles in a highly dynamic manner. In this review, we analyze the proteins involved in the interaction between mitochondria and other cellular organelles, especially the endoplasmic reticulum, lipid droplets, and lysosomes. Recent results indicate that, on one hand, metabolic alterations perturb the interaction between mitochondria and other organelles, and, on the other hand, that deficiency in proteins involved in the tethering between mitochondria and the ER or in specific functions of the interaction leads to metabolic alterations in a variety of tissues. The interaction between organelles is an emerging field that will permit to identify key proteins, to delineate novel modulation pathways, and to elucidate their implications in human disease.

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Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 75%

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 99%

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 99%

Section: Metabolic Impact Of Alterations In Proteins Participating Inmentioning

confidence: 99%

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Metabolic implications of organelle–mitochondria communication

2019

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“…The protein levels of cyclin D1, cyclin E, CDK2, CDK4, Ki-67 and PCNA were decreased in shRNA-VCP-transfected cells [26]. Moreover, ER stress marker levels were increased in Bap31 knockout mice after tunicamycin injection compared with those in control mice [35]. The depletion of VCP by siRNA induces ER stress and the unfolded protein response (UPR) [36].…”

Section: Discussionmentioning

confidence: 95%

B-Cell Receptor-Associated Protein 31 Regulates the Expression of Valosin-Containing Protein Through Elf2

Jia

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: B-cell receptor-associated protein 31 (Bap31) is an evolutionarily conserved, ubiquitously expressed, polytopic integral membrane protein in the endoplasmic reticulum (ER) that is involved in the regulation of apoptosis, protein transport and degradation. Patients with Bap31 mutations exhibit symptoms similar to those exhibited by patients with central nervous system (CNS) diseases, such as deafness, dystonia, and intellectual disability. The present study aimed to investigate the function of Bap31 in CNS diseases by identifying a CNS disease-related gene regulated by Bap31 and exploring the underlying molecular mechanism. Methods: ShRNA-Bap31 and siRNA-Bap31 were used to knockdown Bap31 in N₂a cells, and real-time PCR was performed to detect the mRNA levels of genes involved in CNS diseases. Western blot analyses were used to examine the protein levels of the candidate gene (valosin-containing protein, VCP) both in vivo and in vitro. The functions of Bap31 and VCP in mediating the degradation of the hyper-unstable mutant of cystic fibrosis trans-membrane conductance regulator (CFTRΔF508) were studied. Moreover, real-time PCR, Western blot and dual luciferase reporter analyses were conducted to investigate the molecular mechanism by which Bap31 regulates the expression levels of VCP. Results: VCP was identified as a candidate gene based on its differential expression in N₂a cells following both shRNA- and siRNA-mediated knockdown of Bap31. Both the mRNA and protein levels of VCP were regulated by Bap31 in vivo and in vitro. In the ER-associated degradation (ERAD) pathway, Bap31 also regulated VCP expression and caused differences in the binding quantities of CFTRΔF508 and VCP. Furthermore, a transcription factor of VCP (E74-like factor 2, Elf2) was regulated by Bap31, and Elf2 mediated the changes in VCP transcription and expression in cells with altered Bap31 expression. Conclusion: These results indicate that Bap31 regulates the expression of VCP possibly via Elf2 and support the potential molecular function of Bap31 in CNS diseases.

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Map‐based cloning and characterization of YGL22, a new yellow‐green leaf gene in rice (Oryza sativa)

Yan

Dong

et al. 2020

Crop Science

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Leaf‐color mutants have been extensively studied in rice (Oryza sativa L.) and many corresponding genes have been identified and cloned. However, the mechanism of complex leaf‐color mutations requires further study. In this study, we obtained an introgression line (TIL22) from a set of introgression lines raised using African cultivated rice (O. glaberrima Steud.) as the donor parent and O. sativa subsp. indica Teqing as the recipient. Compared with Teqing, TIL22 showed a yellow‐green leaf phenotype at the seedling stage, but the leaves gradually changed to green after the five‐leaf stage. The photosynthetic pigment contents of yellow‐green leaves at the seedling stage were significantly reduced and chloroplast development was retarded compared with those of Teqing. Genetic analysis indicated that the introgression line phenotype was controlled by a single nuclear gene, temporarily designated YGL22. Map‐based cloning and sequence analysis suggested that the candidate gene was likely to be LOC_Os01g15390, which encodes a chloroplast protein. Real‐time quantitative polymerase chain reaction (qPCR) analysis revealed that the YGL22 transcript level was significantly lower in TIL22 than that of Teqing at the seedling stage. We generated the ygl22 knockout mutant using the CRISPR/Cas9 system. The ygl22 mutants showed a similar phenotype to that of TIL22 at the seedling stage, suggesting that YGL22 may be involved in the early development of chloroplasts in rice. In addition, plant height, number of panicles per plant, and grain yield per plant of ygl22 were not significantly affected. The results indicate that YGL22 can be used as a trait marker gene in hybrid rice production.

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Induction of Liver Steatosis in BAP31-Deficient Mice Burdened with Tunicamycin-Induced Endoplasmic Reticulum Stress

Cited by 23 publications

References 41 publications

Metabolic implications of organelle–mitochondria communication

Metabolic implications of organelle–mitochondria communication

B-Cell Receptor-Associated Protein 31 Regulates the Expression of Valosin-Containing Protein Through Elf2

Map‐based cloning and characterization of YGL22, a new yellow‐green leaf gene in rice (Oryza sativa)

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