Abstract
Perkinsus marinus, a protozoan and the causative agent of perkinsosis (dermo disease) is a prevalent parasite found within the eastern oyster (Crassostrea virginica). In this study, we explore metabolic processes of P. marinus cells under lipid-depleted medium conditions to elucidate the interchanging flux of lipid and carbohydrate metabolism. Although P. marinus can synthesize their own lipids from available nutrients, they display a slower growth in medium not supplemented with lipids as opposed to medium with lipids. Under these conditions, using transcriptomics, we surprisingly observed evidence of stimulated lipid degradation through increased transcription of two core β-oxidation pathway enzymes. Simultaneously, phospholipid biosynthetic pathways were downregulated. Metabolomic analysis supported the transcriptomic results. Most fatty acids were decreased in lipid-deplete medium as opposed to lipid-replete medium, and available glucose was fermented to lactate. A significant increase in the cholesterol derivative zymosterol further supported a downregulation of membrane synthesis under the experimental conditions. A robust tricarboxylic acid (TCA) cycle was apparent by enhanced citrate synthase transcription, and a simultaneous reduction in branched chain amino acids. It is concluded that although P. marinus has the capacity for synthesizing its own lipids, it can respond to lipid deprivation in medium by oxidizing readily available stores, and likely transitioning into a resting stage.
Get full access to this article
View all access options for this article.
References
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
