Summary of project PR002562
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002562. The data can be accessed directly via it's Project DOI: 10.21228/M8GJ95 This work is supported by NIH grant, U2C- DK119886. See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR002562 |
| Project DOI: | doi: 10.21228/M8GJ95 |
| Project Title: | Remodeling of Prochlorococcus metabolism during viral infection |
| Project Type: | Marine Microbial Metabolomics |
| Project Summary: | The marine cyanobacterium Prochlorococcus is the most abundant photoautotroph in the world and is a major contributor to oceanic primary productivity. Viruses are important controls on Prochlorococcus populations with up to 10% of Prochlorococcus cells infected. During infection, viruses remodel their host’s metabolic machinery, creating metabolically distinct cells, termed virocells. However, the specific consequences of viral infection on Prochlorococcus metabolism remain poorly understood. Here, we characterize the infection of non-axenic cultures of Prochlorococcus MED4 by the T7-like virus P-SSP7 using a combination of metabolomics, transcriptomics, and population modeling approaches. P-SSP7 infection dramatically altered the metabolome of Prochlorococcus with 25% of metabolites showing differential abundance. Infected cells exhibited decreased carbon fixation and the draw down of intracellular stores of carbon structures and energy such as glycogen and the osmolytes sucrose and aspartic acid. In contrast, another osmolyte, glucosylglycerol, was accumulated in high concentrations and came to dominate the virocell metabolome. Infected cells also experienced pseudocobalamin (pB12) stress, as evidenced by reduced pB12 concentrations, increased expression of genes to synthesize pB12, and depletion of metabolites whose synthesis relies on pB12 including S-adnosylmethionine (SAM) and the antioxidant glutathione. Collectively, our results suggest that the observed metabolic remodeling is driven by the demand for carbon and energy for virion production and infection-induced oxidative stress. Viral infection changes the substrate and vitamin pools provided by Prochlorococcus to the microbial community, potentially altering the speciation and flux of organic matter in marine systems and acting as a selective force on microbial community composition and function. |
| Institute: | University of Washington |
| Department: | School of Oceanography |
| Laboratory: | Ingalls Lab |
| Last Name: | Sacks |
| First Name: | Joshua |
| Address: | Box 355351 School of Oceanography University of Washington, Seattle WA 98115 |
| Email: | jssacks@uw.edu |
| Phone: | 206 221 6750 |
| Funding Source: | Simons Foundation |
| Publications: | Sacks et al. in prep |
Summary of all studies in project PR002562
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST004081 | Remodeling of Prochlorococcus metabolism during viral infection | Prochlorococcus marinus | University of Washington | MS | 2025-08-19 | 1 | 57 | Uploaded data (2.7G)* |
