Inter-Research > MEPS > v507 > p31-38  
MEPS
Marine Ecology Progress Series

via Mailchimp

MEPS 507:31-38 (2014)  -  DOI: https://doi.org/10.3354/meps10842

Dimethylsulfoxide reduction activity is linked to nutrient stress in Thalassiosira pseudonana NCMA 1335

Christopher E. Spiese*, Elvira A. Tatarkov

Department of Chemistry & Biochemistry, Ohio Northern University, 525 South Main St., Ada, OH 45810, USA
*Corresponding author:

ABSTRACT: The response of dimethylsulfoxide (DMSO) reduction activity (DRA) was examined in the marine diatom Thalassiosira pseudonana under nutrient limitation (nitrogen- or vitamin B12-limitation). DRA was higher in nutrient-limited cultures (160 ± 42% of control for N-limited and 168 ± 52% for B12-limited) than controls. The increased DRA is thought to be due to up-regulation of defense/repair enzymes as opposed to increased substrate availability. By supplying a chiral sulfoxide (methylphenylsulfoxide, MPSO), DRA could be tentatively assigned to a methionine sulfoxide reductase B (MsrB) enzyme due to a decrease in the amount of (R)-MPSO present in limited cultures versus control, in a similar fashion to other marine organisms. Cellular dimethylsulfoniopropionate (DMSP) and DMSO contents were also significantly higher under nutrient stress versus control, indicating physiological stress. This is the first time DRA and cellular DMSO concentrations have been shown to increase during stress conditions in a marine alga. Together, these results suggest a role in nutrient-stress management for DRA, and may provide a link between stress at the cellular level and the biogeochemical cycling of sulfur in the marine environment.


KEY WORDS: Sulfur · Nitrogen · Cobalamin · Dimethylsulfide · Diatom · Methionine sulfoxide reductase


Full text in pdf format
Cite this article as: Spiese CE, Tatarkov EA (2014) Dimethylsulfoxide reduction activity is linked to nutrient stress in Thalassiosira pseudonana NCMA 1335. Mar Ecol Prog Ser 507:31-38. https://doi.org/10.3354/meps10842

Export citation
Share:    Facebook - - linkedIn

 Previous article Next article