Dataset Information

Human cytomegalovirus alters the peroxisome proteome

ABSTRACT: Peroxisomes are primarily metabolic organelles with important functions in lipid metabolism, such as fatty acid oxidation and ether phospholipid synthesis (e.g., plasmalogens). Certain viruses, such as human cytomegalovirus (HCMV), hijack organelle functions to facilitate their replication and spread. However, the role of peroxisomes in herpesvirus replication remains elusive. Therefore, we used targeted mass spectrometry to quantify 60 peroxisome proteins through the HCMV infection cycle. We provide two proteomic experiments. The first experiment (raw files labeled as 20180123) is of samples in biological triplicate from uninfected human fibroblasts and infected human fibroblasts at 6, 24, 48, 72, and 120 hours post infection. The second experiment (raw files labeled as 201806) is from uninfected/infected fibroblasts during phosphonoformate (PFA) treatment and fibroblasts infected with UV-treated HCMV.

OTHER RELATED OMICS DATASETS IN: MTBLS652

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human) Human Cytomegalovirus (strain Ad169) (hhv-5) (human Herpesvirus 5)

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Pierre Jean Beltran

LAB HEAD: Ileana Cristea

PROVIDER: PXD009321 | Pride | 2018-10-04

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20180123_PeroxisomePRM_120hpi_1.msf	Msf
	20180123_PeroxisomePRM_120hpi_1.raw	Raw
	20180123_PeroxisomePRM_120hpi_2.msf	Msf
	20180123_PeroxisomePRM_120hpi_2.raw	Raw
	20180123_PeroxisomePRM_120hpi_3.msf	Msf

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Publications

Infection-Induced Peroxisome Biogenesis Is a Metabolic Strategy for Herpesvirus Replication.

Jean Beltran Pierre M PM Cook Katelyn C KC Hashimoto Yutaka Y Galitzine Cyril C Murray Laura A LA Vitek Olga O Cristea Ileana M IM

Cell host & microbe 20180927 4

Viral proteins have evolved to target cellular organelles and usurp their functions for virus replication. Despite the knowledge of these critical functions for several organelles, little is known about peroxisomes during infection. Peroxisomes are primarily metabolic organelles with important functions in lipid metabolism. Here, we discovered that the enveloped viruses human cytomegalovirus (HCMV) and herpes simplex virus type 1 (HSV-1) induce the biogenesis of and unique morphological changes ...[more]

PMID: 30269970

Similar Datasets

Project description:Data-independent acquisition assessment of human fibroblasts and epithelial cells infected with different strains of human cytomegalovirus (HCMV). Viruses are ubiquitous entities that infect organisms across the kingdoms of life. While viruses can infect a range of cells, tissues, and organisms, this aspect is often not explored in cell culture analyses. There is limited information about which infection-induced changes are shared or distinct in different cellular environments. The prevalent pathogen HCMV remodels the structure and function of subcellular organelles and their interconnected networks formed by membrane contact sites (MCSs). A large portion of this knowledge has been derived from fibroblasts infected with a lab-adapted HCMV strain. Here, we assess strain- and cell type-specific alterations in MCSs and organelle remodeling induced by HCMV. Integrating quantitative mass spectrometry, super-resolution microscopy, and molecular virology assays, we compare infections with lab-adapted and low-passage HCMV strains in fibroblast and epithelial cells. We determine that, despite baseline proteome disparities between uninfected fibroblast and epithelial cells, infection induces convergent changes and is remarkably similar. We show that hallmarks of HCMV infection in fibroblasts, mitochondria-ER encapsulations (MENCs) and peroxisome proliferation, are also conserved in infected epithelial and macrophage-like cells. Exploring cell type-specific differences, we demonstrate that fibroblasts rely on endosomal cholesterol transport while epithelial cells rely on cholesterol from the Golgi. Despite these mechanistic differences, infections in both cell types result in phenotypically similar cholesterol accumulation at the viral assembly complex. Our findings highlight the adaptability of HCMV, in that infections can be tailored to the initial cell state by inducing both shared and unique proteome alterations, ultimately promoting a unified pro-viral environment.