Biosynthesis and regulation of carotenoids in Dunaliella: progresses and prospects

Natural carotenoids are high in demand in global market owing to their widespread applications in nutrition, medicine, food coloring agent and cosmetic, as well as to the natural and healthy preference of consumers today. Some strains of Dunaliella are well known for their talent of massive beta-carotene accumulation. Content of the high bioavailability stereoisomer of beta-carotene, the 9-cis stereoisomer, is highest in Dunaliella among all the natural carotenoids sources. These valuable algae have been exploited commercially for beta-carotene-rich Dunaliella powder and natural beta-carotene in many countries since 1980s. However, drawbacks of traditional production methods have hampered the worldwide promotion of carotenoids production with Dunaliella. To shake off the dilemma, complete understanding of carotenogenic mechanism is urgent. Carotenogenic mechanism in Dunaliella is described in present paper, including carotenogenic pathway and its regulation. Generally, it seems that carotenogenic pathway in Dunaliella is close to the one of higher plants. It is known that reactive oxygen species (ROS) were involved in signal transduction for gene activation. Induction of ROS is in parallel with the enhanced beta-carotene accumulation in Dunaliella. It is suggested that ROS trigger massive carotenoids accumulation in Dunaliella. It also revealed that relation may exist between enhanced beta-carotene accumulation and lipid metabolism. For the talent of beta-carotene synthesis, it is possible that Dunaliella massively accumulates beta-carotene and other high-value carotenoids by genetic technologies.     

Polynomial algebra reveals diverging roles of the unfolded protein response in endothelial cells during ischemia–reperfusion injury

The unfolded protein response (UPR) – the endoplasmic reticulum stress response – is found in various pathologies including ischemia–reperfusion injury (IRI). However, its role during IRI is still unclear. Here, by combining two different bioinformatical methods – a method based on ordinary differential equations (Time Series Network Inference) and an algebraic method (probabilistic polynomial dynamical systems) – we identified the IRE1α–XBP1 and the ATF6 pathways as the main UPR effectors involved in cell’s adaptation to IRI. We validated these findings experimentally by assessing the impact of their knock-out and knock-down on cell survival during IRI.