Dengue and Zika Virus Capsid Proteins Contain a Common PEX19-Binding Motif

Farelo, Mafalda A.; Korrou-Karava, Despoina; Brooks, Katrina F.; Russell, Tiffany A.; Maringer, Kevin; Mayerhofer, Peter

doi:10.3390/v14020253

Cited by 7 publications

(3 citation statements)

References 56 publications

(138 reference statements)

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“…Besides virion assembly, the C protein is also known to interact with cellular proteins to play roles in assisting ZIKV replication, modulating cellular metabolism, and antiviral response. The C protein induces the loss of peroxisomes, which have an important role in innate immunity [ 36 ]. It targets the nonsense-mediated mRNA decay (NMD) pathway, a cellular mRNA surveillance mechanism, via interacting with up-frameshift protein 1 (UPF1), a central NMD regulator, and targeting it for degradation [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Zika Virus Induces Degradation of the Numb Protein Required through Embryonic Neurogenesis

Yang

Chang

et al. 2023

Viruses

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Zika virus (ZIKV) is a mosquito-borne flavivirus and causes an infection associated with congenital Zika syndrome and Guillain–Barre syndrome. The mechanism of ZIKV-mediated neuropathogenesis is not well understood. In this study, we discovered that ZIKV induces degradation of the Numb protein, which plays a crucial role in neurogenesis by allowing asymmetric cell division during embryonic development. Our data show that ZIKV reduced the Numb protein level in a time- and dose-dependent manner. However, ZIKV infection appears to have minimal effect on the Numb transcript. Treatment of ZIKV-infected cells with a proteasome inhibitor restores the Numb protein level, which suggests the involvement of the ubiquitin–proteasome pathway. In addition, ZIKV infection shortens the half-life of the Numb protein. Among the ZIKV proteins, the capsid protein significantly reduces the Numb protein level. Immunoprecipitation of the Numb protein co-precipitates the capsid protein, indicating the interaction between these two proteins. These results provide insights into the ZIKV–cell interaction that might contribute to its impact on neurogenesis.

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Section: Discussionmentioning

confidence: 99%

Zika Virus Induces Degradation of the Numb Protein Required through Embryonic Neurogenesis

Yang

Chang

et al. 2023

Viruses

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“…Besides virion assembly, the C protein is also known to interact with cellular proteins to play roles in assisting ZIKV replication, modulating cellular metabolism, and antiviral response. The C protein induces the loss of peroxisomes, which have an important role in innate immunity [28]. It targets the nonsense-mediated mRNA decay (NMD) pathway, a cellular mRNA surveillance mechanism, via interacting with upframeshift protein 1 (UPF1), a central NMD regulator, and targeting it for degradation [29].…”

Section: Discussionmentioning

confidence: 99%

Zika Virus Induces the Degradation of the Numb Protein that is Required through Embryonic Neurogenesis

He¹,

Yang²,

Chang³

et al. 2023

Preprint

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Zika virus (ZIKV) is a mosquito-borne flavivirus and causes an infection that is associated with neurological manifestations, including microcephaly and Guillain-Barre syndrome. The mechanism of ZIKV-mediated neuropathogenesis is not well understood. In this study, we discovered that ZIKV induces the degradation of the Numb protein, which plays a crucial role in neurogenesis by allowing asymmetric cell division during embryonic development. Our data show that ZIKV reduced the Numb protein level in a time- and dose-dependent manner. However, ZIKV infection appears to have minimal effect on the Numb transcript. Treatment of ZIKV-infected cells with a proteasome inhibitor restores the Numb protein level, which suggests the involvement of the ubiquitin-proteasome pathway. In addition, ZIKV infection shortens the half-life of the Numb protein. Among the ZIKV proteins, the capsid protein significantly reduces the Numb protein level. Immunoprecipitation of the Numb protein co-precipitates the capsid protein, indicating the interaction between these two proteins. These results provide insights into the ZIKV-cell interaction that might contribute to its impact on neurogenesis.

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“…ZIKV viral protease complex NS2A has been shown to localize at peroxisomes and interact with both PEX19 and PEX3 (475). The capsid proteins of DENV, WNV and ZIKV were found to form a stable complex with PEX19 (473,476), and overexpression of the ZIKV capsid protein alone was shown to decrease PEX19 protein levels and peroxisome number. It has been proposed that these viruses evade the peroxisomal antiviral signaling by capsid protein-mediated sequestration and/or degradation of PEX19 (473).…”

Section: Dengue West Nile and Zika Virusesmentioning

confidence: 99%

The physiological functions of human peroxisomes

Wanders

Baes

Ribeiro

et al. 2023

Physiological Reviews

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Peroxisomes are subcellular organelles which play a central role in human physiology by catalyzing a range of unique metabolic functions. The importance of peroxisomes for human health is exemplified by the existence of a group of usually severe diseases caused by an impairment in one or more peroxisomal functions. Among others these include the Zellweger spectrum disorders, X-linked adrenoleukodystrophy and Refsum disease. In order to fulfill their role in metabolism, peroxisomes require the continued interaction with other subcellular organelles including lipid droplets, lysosomes, the endoplasmic reticulum, and mitochondria. In recent years it has become clear that the metabolic alliance between peroxisomes and other organelles requires the active participation of tethering proteins to bring the organelles physically closer together thereby achieving efficient transfer of metabolites. This review intends to describe the current state of knowledge about the metabolic role of peroxisomes in humans with particular emphasis on the metabolic partnership between peroxisomes and other organelles and the consequences of genetic defects in these processes. We will also describe the biogenesis of peroxisomes and the consequences of the multiple genetic defects therein. In addition, we will discuss the functional role of peroxisomes in different organs and tissues and will include relevant information derived from model systems notably peroxisomal mouse models. Finally, we will pay particular attention to a hitherto underrated role of peroxisomes in viral infections.

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Dengue and Zika Virus Capsid Proteins Contain a Common PEX19-Binding Motif

Cited by 7 publications

References 56 publications

Zika Virus Induces Degradation of the Numb Protein Required through Embryonic Neurogenesis

Zika Virus Induces Degradation of the Numb Protein Required through Embryonic Neurogenesis

Zika Virus Induces the Degradation of the Numb Protein that is Required through Embryonic Neurogenesis

The physiological functions of human peroxisomes

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