Abiodun, B. A. | bioRxiv Science

bioRxiv2025

The ornithine-arginine cycle supported a toxic, metalimnic Planktothrix rubescens bloom

Planktothrix rubescens is distinct from other cyanobacterial harmful algal bloom (cHAB) genera: the crimson-red cHAB thrives in the cold, low-light, nutrient-limited metalimnion. Studies have attributed this ecological success to buoyancy regulation, low-light adaptations, and the uptake of nitrogen-rich amino acids. Yet, it remains to be mechanistically determined how this cHAB maintains physiological nutrient quotas in the metalimnion due to limited in situ molecular studies. We employed metagenomics and metabolomics to investigate a toxigenic P. rubescens bloom in Meads Quarry (Knoxville, TN, USA) observed in two separate years. Our results suggest a perennial, metalimnic P. rubescens population may exist, with spring turnover facilitating seasonal migration to the epilimnion. Although P. rubescens dominated the epilimnion and metalimnion, intracellular metabolite pools grouped by depth and suggested depth-discrete partitioning of the arginine deiminase-mediated ornithine-arginine cycle (OAC, i.e., urea cycle). While the arginine influx driving the OAC is unclear, we hypothesize this input is provided via the uptake of urea or nitrogen-rich amino acids. Further, we demonstrate arginine deiminase (argE) is broadly distributed in Planktothrix genera and known microcystin producers, suggesting argE-mediated arginine recycling via the OAC may influence the fitness of toxigenic cHAB genera which require ample nitrogen to synthesize microcystins. Cumulatively, our results serve as a case study to provide insight on the metabolic pathways driving the ecological success of metalimnic P. rubescens blooms. On a broader scale, this work strengthens the case that alternative nitrogen metabolism - including urea utilization, amino acid uptake, and the OAC - is a driver of toxigenic cyanobacterial blooms in fresh waters.

bioinformatics↗

bioRxiv2024

Specific Bacterial Taxa and Their Metabolite, DHPS, Linked to Alzheimers Disease, Parkinsons Disease, and Amyotrophic Lateral Sclerosis.

Neurodegenerative diseases (NDDs) are multifactorial disorders frequently associated with gut dysbiosis, oxidative stress, and inflammation; however, the pathophysiological mechanisms remain poorly understood. We investigated bacterial and metabolic dyshomeostasis in the gut microbiome associated with early disease stages across three NDDs, amyotrophic lateral sclerosis (ALS), Alzheimers Disease (AD), Parkinsons Disease (PD), and healthy controls (HC) and discovered a previously unrecognized link between a microbial-derived metabolite with an unknown role in human physiology, 2,3-dihydroxypropane-1-sulfonate (DHPS), and NDDs. DHPS was downregulated in AD, ALS, and PD, while Eubacterium and Desulfovibrio, capable of metabolizing this metabolite,1-4 were increased in all disease cohorts. Additionally, select taxa within the Clostridia class had strong negative correlations to DHPS suggesting a potential role in DHPS metabolism. Hydrogen sulfide is a catabolic product of DHPS,1,5 and hydrogen sulfide promotes inflammation,6-8 oxidative stress,9 mitochondrial damage,10 and gut dysbiosis,2,11 known hallmarks of NDD. These findings suggest that cryptic sulfur metabolism via DHPS is a missing link in our current understanding of NDD onset and progression. To the best of our knowledge, we are the first to provide evidence of a conserved gut-brain axis linkage of specific bacterial taxa and their metabolism of DHPS shared by three neurodegenerative diseases.

neuroscience↗