Duck PIAS2 negatively regulates RIG-I mediated IFN-β production by interacting with IRF7

Zu, Shaopo; Xue, Qian; He, Zhuoliang; Shi, Chenxi; Wu, Wenbo; Zhang, Junsheng; Li, Weiqiang; Huang, Jianni; Jiao, Peirong; Liao, Ming

doi:10.1016/j.dci.2020.103664

Cited by 7 publications

(6 citation statements)

References 34 publications

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“…Another gene, MEX3C , which is also linked to fat deposition and muscle development and whose function appears to be highly conserved in multiple species ( 69 – 71 ) is also predicted to be impacted in both peregrines and Altai-haplotype carriers (Table S6). PIAS2 is reportedly associated with the immune response to viral infections in ducks ( 72 ). In PIAS2 a missense variant was identified in Altai-haplotype carriers, and a nonsense mutation (stop-loss) was fixed in peregrines (Table S6).…”

Section: Resultsmentioning

confidence: 99%

Genomic, genetic and phylogenetic evidence for a new falcon species using chromosome-level genome assembly of the gyrfalcon and population genomics

Al-Ajli

Formenti

Fédrigo

et al. 2023

Preprint

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The taxonomic classification of a falcon population found in the Altai region in Asia has been heavily debated for two centuries and previous studies have been inconclusive, hindering a more informed conservation approach. Here, we generated a chromosome-level gyrfalcon reference genome using the Vertebrate Genomes Project (VGP) assembly pipeline. Using whole genome sequences of 44 falcons from different species and populations, including "Altai" falcons, we analyzed their population structure, admixture patterns and demographic history. We find that the Altai falcons are genomically mosaic of saker and gyrfalcon ancestries, and carry distinct W- and mitochondrial-haplotypes that cluster with the lanner falcon. The Altai haplotype diverged 422,000 years ago from the ancestor of sakers and gyrfalcons, both of which, in turn, split 109,000 years ago. The Altai W chromosome includes coding variants that may influence important structural, behavioral and reproductive traits. These findings support the designation of Altai falcons as a distinct falcon species (Falco altaicus).

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Section: Resultsmentioning

confidence: 99%

Genomic, genetic and phylogenetic evidence for a new falcon species using chromosome-level genome assembly of the gyrfalcon and population genomics

Al-Ajli

Formenti

Fédrigo

et al. 2023

Preprint

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“…Among the confirmed genes in the type I IFN signaling pathway, we identified PIAS2, the specific negative regulator of the IFNβ-IFNAR signaling [ 22 ], i.e., via specific inhibition of STAT2 [ 21 ] to impact the survival and function of neurons. Moreover, PIAS2 was significantly raised in neurons in the brains of sPD, and in particular in sPDD patients, paralleling our finding in Ifnb −/− mice.…”

Section: Discussionmentioning

confidence: 99%

“…Protein inhibitor of STAT2 (PIAS2) is a negative regulator of STAT [ 21 ] and IFN-β signaling [ 22 ] and has SUMO E3 ligase activity [ 23 ]. PIAS2 was recently shown to stabilize α-syn by counteracting its ubiquitin-mediated degradation, promoting its intracellular aggregation [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

PIAS2-mediated blockade of IFN-β signaling: a basis for sporadic Parkinson disease dementia

et al. 2021

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Familial Parkinson disease (PD) is associated with rare genetic mutations, but the etiology in most patients with sporadic (s)PD is largely unknown, and the basis for its progression to dementia (sPDD) is poorly characterized. We have identified that loss of IFNβ or IFNAR1, the receptor for IFNα/β, causes pathological and behavioral changes resembling PDD, prompting us to hypothesize that dysregulated genes in IFNβ-IFNAR signaling pathway predispose one to sPD. By transcriptomic analysis, we found defective neuronal IFNβ-IFNAR signaling, including particularly elevated PIAS2 associated with sPDD. With meta-analysis of GWASs, we identified sequence variants in IFNβ-IFNAR-related genes in sPD patients. Furthermore, sPDD patients expressed higher levels of PIAS2 mRNA and protein in neurons. To determine its function in brain, we overexpressed PIAS2 under a neuronal promoter, alone or with human α-synuclein, in the brains of mice, which caused motor and cognitive impairments and correlated with intraneuronal phosphorylated (p)α-synuclein accumulation and dopaminergic neuron loss. Ectopic expression of neuronal PIAS2 blocked mitophagy, increased the accumulation of senescent mitochondrial and oxidative stress, as evidenced by excessive oxDJ1 and 8OHdG, by inactivating ERK1/2-P53 signaling. Conversely, PIAS2 knockdown rescued the clinicopathological manifestations of PDD in Ifnb–/– mice on restoring mitochondrial homeostasis, oxidative stress, and pERK1/2-pP53 signaling. The regulation of JAK-STAT2-PIAS2 signaling was crucial for neurite outgrowth and neuronal survival and excitability and thus might prevent cognitive impairments. Our findings provide insights into the progression of sPD and dementia and have implications for new therapeutic approaches.

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“…Luciferase activity was measured by a Promega Glomax 96 microplate luminometer. The relative luciferase activity was calculated by the ratio of firefly to Renilla luciferase activity as previously described (20). All reporter assays were repeated three times independently and three replicate wells were done in each assay.…”

Section: Luciferase Reporter Gene Assaysmentioning

confidence: 99%

Duck TRIM29 negatively regulates type I IFN production by targeting MAVS

Song

et al. 2023

Front. Immunol.

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The innate immune response is a host defense mechanism that induces type I interferon and proinflammatory cytokines. Tripartite motif (TRIM) family proteins have recently emerged as pivotal regulators of type I interferon production in mammals. Here, we first identified duck TRIM29, which encodes 571 amino acids and shows high sequence homology with other bird TRIM29 proteins. DuTRIM29 inhibited IFN-β and IRF7 promoter activation in a dose-dependent manner and downregulated the mRNA expression of IFN-β, IRF7, Mx and IL-6 mediated by duRIG-I. Moreover, duTRIM29 interacted and colocalized with duMAVS in the cytoplasm. DuTRIM29 interacted with duMAVS via its C-terminal domains. In addition, duTRIM29 inhibited IFN-β and IRF7 promoter activation and significantly downregulated IFN-β and immune-related gene expression mediated by duMAVS in ducks. Furthermore, duTRIM29 induced K29-linked polyubiquitination and degradation of duMAVS to suppress the expression of IFN-β. Overall, our results demonstrate that duTRIM29 negatively regulates type I IFN production by targeting duMAVS in ducks. This study will contribute to a better understanding of the molecular mechanism regulating the innate immune response by TRIM proteins in ducks.

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Duck PIAS2 negatively regulates RIG-I mediated IFN-β production by interacting with IRF7

Cited by 7 publications

References 34 publications

Genomic, genetic and phylogenetic evidence for a new falcon species using chromosome-level genome assembly of the gyrfalcon and population genomics

Genomic, genetic and phylogenetic evidence for a new falcon species using chromosome-level genome assembly of the gyrfalcon and population genomics

PIAS2-mediated blockade of IFN-β signaling: a basis for sporadic Parkinson disease dementia

Duck TRIM29 negatively regulates type I IFN production by targeting MAVS

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