Search bioRxiv⌕ Search

bioRxiv · 10.1101/2022.01.24.477214

Transforming chemical proteomics enrichment into high throughput method using SP2E workflow.

Abstract

Protein post-translational modifications (PTMs) play a critical role in the regulation of protein catalytic activity, localization and protein-protein interactions. Attachment of PTMs onto proteins significantly diversifies their structure and function resulting in so-called proteoforms. However, the sole identification of post-translationally modified proteins, which are often cell type and disease specific, is still a highly challenging task. Sub-stoichiometric amounts and modification of low abundant proteins necessitate purification or enrichment of the modified proteins. Although the introduction of the mass spectrometry-based chemical proteomic strategies have enabled to screen protein PTMs with increased throughput, sample preparation has remained highly time consuming and tedious. Here, we report an optimized workflow for enrichment of PTM proteins in 96-well plate format which can be possible extended to robotic automatization. This platform allows to significantly lower the input of total protein, which opens up the opportunity to screen specialized and difficult to culture cell lines in high-throughput manner. The presented SP2E protocol is robust, time- and cost-effective as well as suitable for large-scale screening of proteoforms. Application of the SP2E protocol will thus enable the characterization of proteoforms in various processes such as neurodevelopment, neurodegeneration and cancer and may contribute to an overall acceleration of the recently launched Human Proteoform Project.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Becker, T., Wiest, A., Telek, A., Bejko, D., Hoffmann-Roeder, A., Kielkowski, P.. 2022-01-25. Transforming chemical proteomics enrichment into high throughput method using SP2E workflow.. https://doi.org/10.1101/2022.01.24.477214

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Aging Remodels the Female Skeletal Muscle Proteome Toward Matrix, Chromatin and Lysosomal Programs that Track Loss of Physical Function

Loss of skeletal muscle strength and mobility is among the most consequential features of human aging, yet the molecular programs that accompany this decline in women remain poorly understood. Here, we performed deep comprehensive data-independent acquisition (DIA) proteomic profiling of vastus lateralis biopsies from 10 younger (24-30 years) and 10 older (70-84 years) healthy women enrolled through the NIH Common Fund Cellular Senescence Network (SenNet), with matched measurements of grip strength and gait speed. Of 2,391 quantified protein groups, 163 were significantly altered with age, and partial least squares-discriminant analysis completely separated the age groups (cross-validated AUC = 1.00). Older muscle showed increased extracellular matrix and vascular remodeling proteins (TIMP3, COL8A1, ELN, FBN1), nuclear, chromatin and RNA-binding proteins (HMGB1, HMGB2, histone H1.0, MATR3, NCL), and lysosomal and senescence-associated secretory phenotype (SASP)-associated proteins (CTSZ, CTSD, PSAP), together with reduced glycolytic and energetic proteins (GAPDH, ENO3, PHKA1, CYCS). Age effects were robust to adjust for body mass index (BMI). Integrating differential abundance, multivariate importance and participant-level consistency, we defined a 24-protein skeletal muscle aging signature whose score separated all younger from all elderly women. Combining grip strength and gait speed into a combined function score, we found that 23 of the 24 signature proteins correlated with physical function (FDR < 0.05), and the signature score correlated strongly with function (r = -0.79). The senescence-associated alarmins HMGB1 and HMGB2 emerged as lead proteins: HMGB1 showed the strongest association with function (r = -0.86), and both remained associated after adjustment for age group. Together, these data define a senotype proteomic program in aging female skeletal muscle and a molecular signature of muscle function that, after validation, may serve as a readout for interventions that aim to preserve physical performance in elderly women.

biochemistry↗

SUMOylation Regulates IRF2BP2 Nuclear Localization and Stability

Interferon Regulatory Factor-2 Binding Protein 2 (IRF2BP2) is a transcriptional cofactor implicated in diverse biological processes. Although it functions primarily as a repressor, it can also activate gene expression. However, the mechanisms governing IRF2BP2 regulation remain poorly understood. Here, we demonstrate that IRF2BP2 interacts with UBE2I, the SUMO E2 ligase, and undergoes multi-SUMOylation, which enhances its nuclear localization. We further show that IRF2BP2 nuclear import is importin-{beta}-dependent and requires the functional nuclear localization signal (NLS). IRF2BP2 preferentially accumulates in transcriptionally active euchromatin in both resting and S-phase cells, consistent with its role in transcriptional control. We further reveal that SUMOylation contributes to IRF2BP2 stability. Moreover, IRF2BP2 is also ubiquitinated, predominantly through K6-linked ubiquitin chains, a non-proteolytic modification that aligns with our observation that IRF2BP2 is not degraded by the proteasome. Together, these findings identify SUMOylation and non-proteolytic ubiquitination as key mechanisms regulating IRF2BP2, highlighting a novel SUMO1-NLS-importin-{beta}-dependent pathway that governs its localization.

biochemistry↗

S-adenosylmethionine supply controls DNA methylation turnover in synovial sarcoma

Background: Methionine is the nutrient source of the metabolite S-adenosylmethionine (SAM) used to methylate chromatin for regulation of gene expression. Disruptions to this metabolic supply, including nutritional deficiency of certain B vitamins, alter chromatin methylation and have been implicated in tumor growth. Objective: To define how cellular SAM supply controls DNA methylation dynamics and the disruption of oncogenic gene expression in synovial sarcoma. Methods: Cell line models of synovial sarcoma were treated with the DNA methyltransferase inhibitor azacitidine or the small-molecule MAT2A inhibitor AG-270, which blocks SAM synthesis from methionine. Intracellular SAM concentrations were quantified by liquid chromatography-mass spectrometry. Global DNA methylation rates were measured by stable isotope tracing with [2H3-methyl]-methionine. Genomic sites of altered DNA methylation were identified by EM-seq and the associated transcriptional changes measured by RNA-seq. Results: Inhibition of SAM synthesis reduced intracellular SAM concentration from 94 uM to 5.6 uM (p value < 0.0001) at 24 hours. This was associated with a 19% decrease (p value < 0.0001) in the global 5-methyldeoxycytosine turnover rate, while total DNA methylation levels were maintained. In contrast to the global DNA hypomethylation induced by azacitidine, SAM depletion resulted in a redistribution of DNA methylation with loss at 252 and gain at 206 genomic sites, and the transcriptional response to SAM depletion was not associated with changes in promoter methylation at the altered genes. Both azacitidine and SAM depletion activated mesenchymal genes, while suppressing cell cycle progression. Conclusions: Metabolic supply of SAM is a major regulator of DNA methylation turnover providing a mechanism by which nutritional or genetic disruptions to SAM metabolism can alter chromatin methylation and gene expression.

biochemistry↗