Dataset Information

Mapping the interactome of OCIAD1 in human K562 cells

ABSTRACT: Immunoprecipitation of OCIAD1 followed by mass spectrometry analysis to identify binding partners in human cells. To determine the functional significance of OCIAD1 interactors, we also looked for interactions that were modulated by a loss-of-function mutant (F102A).

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Maxence Le Vasseur

LAB HEAD: Jodi Nunnari

PROVIDER: PXD025682 | Pride | 2021-05-14

REPOSITORIES: Pride

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			Action	DRS
	20201028_u2os_cell_mito_gpf_spectral_lib.tsv.speclib	Tabular
	FL08032020_97_MAX2.raw	Raw
	FL08102020_12_MAX10.raw	Raw
	FL08102020_18_MAX6.raw	Raw
	FL08102020_20_MAX11.raw	Raw

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Project description:Endometriosis is a debilitating gynecological disorder affecting approximately 10% of the female population. Despite its prevalence, robust methods to classify and treat endometriosis remain elusive. Changes throughout the menstrual cycle in tissue size, architecture, cellular composition, and individual cell phenotypes make it extraordinarily challenging to identify markers or cell types associated with uterine pathologies since disease-state alterations in gene and protein expression are convoluted with cycle phase variations. Here, we developed an integrated workflow to generate both proteomic and single-cell RNA-sequencing (scRNA-seq) data sets using tissues and cells isolated from the uteri of control and endometriotic donors. Using a linear mixed effect model (LMM), we identified proteins associated with cycle stage and disease, revealing a set of genes that drive separation across these two biological variables. Further, we analyzed our scRNA-seq data to identify cell types expressing cycle and disease- associated genes identified in our proteomic data. A module scoring approach was used to identify cell types driving the enrichment of certain biological pathways, revealing several pathways of interest across different cell subpopulations. Finally, we identified ligand-receptor pairs including Axl/Tyro3 – Gas6, that may modulate interactions between endometrial macrophages and/or endometrial stromal/epithelial cells. Analysis of these signaling pathways in an independent cohort of endometrial biopsies revealed a significant decrease in Tyro3 expression in patients with endometriosis compared to controls, both transcriptionally and through histological staining. This measured decrease in Tryo3 in patients with disease could serve as a novel diagnostic biomarker or treatment avenue for patients with endometriosis. Taken together, this integrated approach provides a framework for integrating LMMs, proteomic and RNA-seq data to deconvolve the complexities of complex uterine diseases and identify novel genes and pathways underlying endometriosis.

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Mapping the interactome of OCIAD1 in human K562 cells

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