Dataset Information

Proteome analysis of bacterial strain Thermodesulfobium acidiphilum

ABSTRACT: Proteome analysis of bacterial strain Thermodesulfobium acidiphilum 3127-1 was done using off-line SCX fractionation of tryptic peptides with subsequent LC-MS/MS analyses of obtained fractions using Q Exactive HF mass spectrometer.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Thermodesulfobium Acidiphilum

SUBMITTER: Rustam Ziganshin

LAB HEAD: Elizaveta A. Bonch-Osmolovskaya

PROVIDER: PXD014169 | Pride | 2019-08-19

REPOSITORIES: Pride

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Publications

Form III RubisCO-mediated transaldolase variant of the Calvin cycle in a chemolithoautotrophic bacterium.

Frolov Evgenii N EN Kublanov Ilya V IV Toshchakov Stepan V SV Lunev Evgenii A EA Pimenov Nikolay V NV Bonch-Osmolovskaya Elizaveta A EA Lebedinsky Alexander V AV Chernyh Nikolay A NA

Proceedings of the National Academy of Sciences of the United States of America 20190826 37

The Calvin-Benson-Bassham (CBB) cycle assimilates CO<sub>2</sub> for the primary production of organic matter in all plants and algae, as well as in some autotrophic bacteria. The key enzyme of the CBB cycle, ribulose-bisphosphate carboxylase/oxygenase (RubisCO), is a main determinant of de novo organic matter production on Earth. Of the three carboxylating forms of RubisCO, forms I and II participate in autotrophy, and form III so far has been associated only with nucleotide and nucleoside meta ...[more]

PMID: 31451656

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Project description:Neurologic manifestations are among the most frequently reported complications of COVID-19. However, given the paucity of tissue samples and highly infectious nature of the etiologic agent of COVID-19, we have limited information to understand the neuropathogenesis of COVID-19. Therefore to better understand the impact of COVID-19 in brain, we employed mass-spectrometry-based proteomics using data-independent acquisition mode (DIA) to investigate cerebrospinal fluid (CSF) proteins collected from two different non-human primates, Rhesus Macaque and African Green Monkeys for the neurologic effects of the infection. These monkeys exhibited minimal to mild pulmonary pathology but moderate to severe CNS pathology. Our results indicate that CSF proteome changes after infection resolution correspond with bronchial virus abundance during early infection and revealed substantial differences between the infected NHPs and their age-matched uninfected controls, suggesting these differences could reflect altered secretion of CNS factors in response to SARS-CoV-2-induced neuropathology. We also observed the infected animals to exhibit much scattered data distributions as compared to the tightly clustered corresponding controls which suggest the heterogeneity of the CSF proteome change and the host response to the viral infection. In addition, dysregulated CSF proteins were preferentially enriched in functional pathways associated with progressive neurodegenerative disorders, hemostasis and innate immune responses that could influence neuroinflammatory responses following COVID-19. Mapping dysregulated proteins to the Human Brain Protein Atlas found that these proteins tended to be enriched in brain regions that exhibit more frequent injury following COVID-19. It therefore appears reasonable to speculate that such CSF protein changes could serve as signatures for neurologic injury, identify important regulatory pathways in this process, and potentially reveal therapeutic targets to prevent or attenuate the development of neurologic injuries following COVID-19.

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