The Carotenogenesis Pathway via the Isoprenoid-I2-carotene Interference Approach in a New Strain of Dunaliella salina Isolated from Baja California Mexico

• Published in: Marine drugs 2009-03, Vol.7 (1), p.45-56
• Main Authors: Paniagua-Michel, J, Capa-Robles, Willian, Olmos-Soto, Jorge, Gutierrez-Millan, Luis Enrique
• Format: Article
• Language: English
• Subjects: Dunaliella salina; Marine; Salina
• ISSN: 1660-3397; 1660-3397
• DOI: 10.3390/md7010045

D. salina is one of the recognized natural sources to produce I2-carotene, and an useful model for studying the role of inhibitors and enhancers of carotenogenesis. However there is little information in D. salina regarding whether the isoprenoid substrate can be influenced by stress factors (carotenogenic) or selective inhibitors which in turn may further contribute to elucidate the early steps of carotenogenesis and biosynthesis of I2-carotene. In this study, Dunaliella salina (BC02) isolated from La Salina BC Mexico, was subjected to the method of isoprenoids-I2-carotene interference in order to promote the interruption or accumulation of the programmed biosynthesis of carotenoids. When Carotenogenic and non-carotenogenic cells of D. salina BC02 were grown under photoautotrophic growth conditions in the presence of 200 AmM fosmidomycin, carotenogenesis and the synthesis of I2-carotene were interrupted after two days in cultured D. salina cells. This result is an indirect consequence of the inhibition of the synthesis of isoprenoids and activity of the recombinant DXR enzyme thereby preventing the conversion of 1-deoxy-D-xylulose 5-phosphate (DXP) to 2-C-methyl-D-erythritol (MEP) and consequently interrupts the early steps of carotenogenesis in D. salina. The effect at the level of proteins and RNA was not evident. Mevinolin treated D. salina cells exhibited carotenogenesis and I2-carotene levels very similar to those of control cell cultures indicating that mevinolin not pursued any indirect action in the biosynthesis of isoprenoids and had no effect at the level of the HMG-CoA reductase, the key enzyme of the Ac/MVA pathway.