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SIRT3 interactions and mitochondrial proteome during HCMV infection

ABSTRACT: SIRT3 has been shown to inhibit HCMV infection, but the mechanism under the antiviral effect is not clear. To identify the mediator of SIRT3 antiviral function, we aim to identify and quantify SIRT3 interactions during HCMV infection. A set of large-scale IPs were performed to determine the specific interactions with SIRT3 during infection, while small-scale IPs were conducted to determine the temporal interactions over the life cycle of infection. The mitochondrial proteome was used to characterize the changes of protein abundances after infection, and it was used for the normalization of acetylation.

INSTRUMENT(S): LTQ Orbitrap Velos, Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Lung, Fibroblast

SUBMITTER: Xinlei Sheng

LAB HEAD: Ileana M. Cristea

PROVIDER: PXD018995 | Pride | 2021-04-01

REPOSITORIES: Pride

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Project description:Hypersensitive response-related programmed cell death (PCD) has been extensively analyzed in various plant–virus interactions. However, little is known about changes in gene expression associated with cell death caused by compatible viruses. The synergistic interaction of Potato virus X (PVX) with Plum pox virus (PPV) results in increased symptoms that lead to systemic necrosis (SN) in Nicotiana benthamiana. Here, we performed three transcriptome comparisons in response to i) a PVX recombinant virus expressing the helper component-proteinase (HC-Pro) gene from PPV that leads to SN, ii) a systemic incompatible interaction conferred by the Tobacco mosaic virus (TMV)-resistance gene N (SHR), and iii) the depletion of the PBE subunit of the proteasome that leads to PCD by virus induced gene silencing (VIGS Prot), at early and late stages of infection. Our analysis indicated that the SN response was clustered with SHR by the similarity of their overall gene expression profiles. However, the expression profiles of defence-related and hormone-responsive genes in response to SN were more closely related to the response to VIGS Prot than to that elicited by SHR. This suggests the potential contribution of proteasome dysfunction to the increase in pathogenicity observed in PVX-potyvirus infections We compare the gene expression profiles of Nicotiana benthamiana plants infected with either necrosis-inducing viruses or non-necrosis-inducing viruses, as follow: PVX/HCWT-infected plants versus plants infected with a PVX recombinant virus expressing a PPV HC-Pro mutant (PVX/HCLH) that was unable to induce the SN response (SN comparison), at 7 and 11 days postinoculation (dpi), (ii) TRV:NbPBE-silenced plants versus plants infected with the TRV empty vector (VIGS Prot comparison), at 4 and 8 days after infiltration (dpa), and (iii) TMV-GFP-infected, N-transgenic plants versus wild-type plants infected with TMV-GFP (SHR comparison), at 24 and 72 hours after temperature shift (hts). Per time and treatment, three independent biological replicates were used to monitor differences in gene expression between treatments

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SIRT3 interactions and mitochondrial proteome during HCMV infection

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