Marine diatoms have recently gained much attention as they are expected to be a promising resource for sustainable production of bioactive compounds such as carotenoids and biofuels as a future clean energy solution. To develop photosynthetic cell factories, it is important to improve diatoms for value-added products. In this study, we utilized UVC radiation to induce mutations in the marine diatom Phaeodactylum tricornutum and screened strains with enhanced accumulation of neutral lipids and carotenoids. Adaptive laboratory evolution (ALE) was also used in parallel to develop altered phenotypic and biological functions in P. tricornutum and it was reported for the first time that ALE was successfully applied on diatoms for the enhancement of growth performance and productivity of value-added carotenoids to date. Liquid chromatography-mass spectrometry (LC-MS) was utilized to study the composition of major pigments in the wild type P. tricornutum, UV mutants and ALE strains. UVC radiated strains exhibited higher accumulation of fucoxanthin as well as neutral lipids compared to their wild type counterpart. In addition to UV mutagenesis, P. tricornutum strains developed by ALE also yielded enhanced biomass production and fucoxanthin accumulation under combined red and blue light. In short, both UV mutagenesis and ALE appeared as an effective approach to developing desired phenotypes in the marine diatoms via electromagnetic radiation-induced oxidative stress.

Diatoms are a major group of unicellular algae that are rich in lipids and carotenoids. However, sustained research efforts are needed to improve the strain performance for high product yields towards commercialization. In this study, we generated a number of mutants of the model diatom Phaeodactylum tricornutum, a cosmopolitan species that has also been found in Nordic region, using the chemical mutagens ethyl methanesulfonate (EMS) and N-methyl-N′-nitro-N-nitrosoguanidine (NTG). We found that both chlorophyll a and neutral lipids had a significant correlation with carotenoid content and these correlations were better during exponential growth than in the stationary growth phase. Then, we studied P. tricornutum common metabolic pathways and analyzed correlated enzymatic reactions between fucoxanthin synthesis and pigmentation or lipid metabolism through a genome-scale metabolic model. The integration of the computational results with liquid chromatography-mass spectrometry data revealed key compounds underlying the correlative metabolic pathways. Approximately 1000 strains were screened using fluorescence-based high-throughput method and five mutants selected had 33% or higher total carotenoids than the wild type, in which four strains remained stable in the long term and the top mutant exhibited an increase of 69.3% in fucoxanthin content compared to the wild type. The platform described in this study may be applied to the screening of other high performing diatom strains for industrial applications.

Background and objective: Osteosarcopenia, a comorbidity of osteoporosis and sarcopenia in the elderly, involves bone-muscle crosstalk, but its core molecular mechanism remains unclear. miR-206 is traditionally considered muscle-specific; this study explores miR-206-3p’s expression in musculoskeletal tissue and correlation with clinical parameters. Methods: A prospective cohort of 158 elderly hip fracture patients (79 osteosarcopenia, 79 controls) was enrolled. qRT-PCR, in situ hybridization, and scRNA-seq were used to analyze miR-206-3p’s expression, distribution, and cell specificity. Correlations with grip strength, gait speed, and BMD were assessed. Results: miR-206-3p was significantly downregulated in both tissues of the osteosarcopenia group (P < 0.001), highly expressed in Myod1⁺ muscle satellite cells and Runx2⁺ osteoprogenitor cells (> 82%), and weakly in mature cells (< 12%). It positively correlated with grip strength, gait speed, and BMD (r = 0.562–0.682, P < 0.001). Conclusion: miR-206-3p is co-expressed in bone-muscle progenitor cells, with synchronous downregulation linked to functional decline, challenging its "muscle-specific" notion and serving as a key molecular hub for bone-muscle crosstalk.