To Ubiquitinate or Not to Ubiquitinate: TRIM17 in Cell Life and Death

Basu-Shrivastava, Meenakshi; Kozoriz, Alina; Desagher, Solange; Lassot, Irina

doi:10.3390/cells10051235

Cited by 9 publications

(9 citation statements)

References 157 publications

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“…Indeed, Trim17 reduces the interaction between Trim39 and NFATc3, as determined by both co-IP of overexpressed proteins and proximity ligation of endogenous proteins (PLA). These results are reminiscent of the effect of TRIM17 on the interaction between TRIM41 or TRIM28 and their respective substrates (Basu-Shrivastava et al, 2021). Further experiments are required to identify the structural determinants of the inhibitory effect of Trim17 on other TRIM proteins.…”

Section: Discussionmentioning

confidence: 95%

“…In previous work, we have shown that NFATc3 can be SUMOylated on three consensus sites (Mojsa et al, 2015). We have also found that NFATc3 binds to Trim17 (Mojsa et al, 2015), which belongs to a large family of RING-containing E3 ubiquitin-ligases (Basu-Shrivastava et al, 2021). Although its E3 ubiquitin-ligase activity has been confirmed (I.…”

Section: Introductionmentioning

confidence: 95%

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Trim39 regulates neuronal apoptosis by acting as a SUMO-targeted E3 ubiquitin-ligase for the transcription factor NFATc3

Basu-Shrivastava

Mojsa

Mora³

et al. 2022

Cell Death Differ

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NFATc3 is the predominant member of the NFAT family of transcription factors in neurons, where it plays a pro-apoptotic role. Mechanisms controlling NFAT protein stability are poorly understood. Here we identify Trim39 as an E3 ubiquitin-ligase of NFATc3. Indeed, Trim39 binds and ubiquitinates NFATc3 in vitro and in cells where it reduces NFATc3 protein level and transcriptional activity. In contrast, silencing of endogenous Trim39 decreases NFATc3 ubiquitination and increases its activity, thereby resulting in enhanced neuronal apoptosis. We also show that Trim17 inhibits Trim39-mediated ubiquitination of NFATc3 by reducing both the E3 ubiquitin-ligase activity of Trim39 and the NFATc3/Trim39 interaction. Moreover, we identify Trim39 as a new SUMO-targeted E3 ubiquitin-ligase (STUbL). Indeed, mutation of SUMOylation sites in NFATc3 or SUMO-interacting motifs in Trim39 reduces NFATc3/Trim39 interaction and Trim39-induced ubiquitination of NFATc3. In addition, Trim39 preferentially ubiquitinates SUMOylated forms of NFATc3 in vitro. As a consequence, a SUMOylation-deficient mutant of NFATc3 exhibits increased stability and pro-apoptotic activity in neurons. Taken together, these data indicate that Trim39 modulates neuronal apoptosis by acting as a STUbL for NFATc3.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 95%

Trim39 regulates neuronal apoptosis by acting as a SUMO-targeted E3 ubiquitin-ligase for the transcription factor NFATc3

Basu-Shrivastava

Mojsa

Mora³

et al. 2022

Cell Death Differ

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“…Moreover, TRIM17 can not only promote the degradation of the anti-apoptotic protein MCL1 but also prevent the ubiquitination of other proteins and stabilize them by binding to other TRIM proteins and inhibiting their E3 ubiquitin ligase activity. This dual action confers several pivotal roles to TRIM17 in crucial cellular processes such as apoptosis and autophagy ( Basu-Shrivastava et al, 2021 ). On the contrary, the MAPK family members have a close relationship with other viral signaling pathways, such as NF-κB, PI3K/Akt, and Janus kinase/signal transducer and activator of transcription (JAK-STAT) ( Chander et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Profile of MA-104 Cell Line Associated With the Pathogenesis of Bovine Rotavirus Strain Circulated in Chinese Calves

Elkady

Chen

et al. 2022

Front. Microbiol.

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Bovine rotavirus (BRV) causes massive economic losses in the livestock industry worldwide. Elucidating the pathogenesis of BRV would help in the development of more effective measures to control BRV infection. The MA-104 cell line is sensitive to BRV and is thereby a convenient tool for determining BRV–host interactions. Thus far, the role of the microRNAs (miRNAs) of MA-104 cells during BRV infection is still ambiguous. We performed Illumina RNA sequencing analysis of the miRNA libraries of BRV-infected and mock-infected MA-104 cells at different time points: at 0 h post-infection (hpi) (just after 90 min of adsorption) and at 6, 12, 24, 36, and 48 hpi. The total clean reads obtained from BRV-infected and uninfected cells were 74,701,041 and 74,184,124, respectively. Based on these, 579 were categorized as known miRNAs and 144 as novel miRNAs. One hundred and sixty differentially expressed (DE) miRNAs in BRV-infected cells in comparison with uninfected MA-104 cells were successfully investigated, 95 of which were upregulated and 65 were downregulated. The target messenger RNAs (mRNAs) of the DE miRNAs were examined by bioinformatics analysis. Functional annotation of the target genes with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) suggested that these genes mainly contributed to biological pathways, endocytosis, apoptotic process, trans-Golgi membrane, and lysosome. Pathways such as the mammalian target of rapamycin (mTOR) (mml-miR-486-3p and mml-miR-197-3p), nuclear factor kappa B (NF-κB) (mml-miR-204-3p and novel_366), Rap1 (mml-miR-127-3p), cAMP (mml-miR-106b-3p), mitogen-activated protein kinase (MAPK) (mml-miR-342-5p), T-cell receptor signaling (mml-miR-369-5p), RIG-I-like receptor signaling (mml-miR-504-5p), AMP-activated protein kinase (AMPK) (mml-miR-365-1-5p), and phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) signaling (mml-miR-299-3p) were enriched. Moreover, real-time quantitative PCR (qPCR) verified the expression profiles of 23 selected DE miRNAs, which were consistent with the results of deep sequencing, and the 28 corresponding target mRNAs were mainly of regulatory pathways of the cellular machinery and immune importance, according to the bioinformatics analysis. Our study is the first to report a novel approach that uncovers the impact of BRV infection on the miRNA expressions of MA-104 cells, and it offers clues for identifying potential candidates for antiviral or vaccine strategies.

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“…The team led by Dr. Solange Desagher at the Institute of Molecular Genetics of Montpellier (IGMM) has been studying the regulation of apoptosis by the E3 ubiquitin-ligase TRIM17 for several years [ 31 ].…”

Section: Team Workmentioning

confidence: 99%

Keeping Cell Death Alive: An Introduction into the French Cell Death Research Network

et al. 2022

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Since the Nobel Prize award more than twenty years ago for discovering the core apoptotic pathway in C. elegans, apoptosis and various other forms of regulated cell death have been thoroughly characterized by researchers around the world. Although many aspects of regulated cell death still remain to be elucidated in specific cell subtypes and disease conditions, many predicted that research into cell death was inexorably reaching a plateau. However, this was not the case since the last decade saw a multitude of cell death modalities being described, while harnessing their therapeutic potential reached clinical use in certain cases. In line with keeping research into cell death alive, francophone researchers from several institutions in France and Belgium established the French Cell Death Research Network (FCDRN). The research conducted by FCDRN is at the leading edge of emerging topics such as non-apoptotic functions of apoptotic effectors, paracrine effects of cell death, novel canonical and non-canonical mechanisms to induce apoptosis in cell death-resistant cancer cells or regulated forms of necrosis and the associated immunogenic response. Collectively, these various lines of research all emerged from the study of apoptosis and in the next few years will increase the mechanistic knowledge into regulated cell death and how to harness it for therapy.

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To Ubiquitinate or Not to Ubiquitinate: TRIM17 in Cell Life and Death

Cited by 9 publications

References 157 publications

Trim39 regulates neuronal apoptosis by acting as a SUMO-targeted E3 ubiquitin-ligase for the transcription factor NFATc3

Trim39 regulates neuronal apoptosis by acting as a SUMO-targeted E3 ubiquitin-ligase for the transcription factor NFATc3

MicroRNA Profile of MA-104 Cell Line Associated With the Pathogenesis of Bovine Rotavirus Strain Circulated in Chinese Calves

Keeping Cell Death Alive: An Introduction into the French Cell Death Research Network

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