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ARS Home » Southeast Area » Gainesville, Florida » Center for Medical, Agricultural and Veterinary Entomology » Chemistry Research » Research » Publications at this Location » Publication #325570

Research Project: Disease Defense Responses Signaling in Maize

Location: Chemistry Research

Title: Maize white seedling 3 results from disruption of homogentisate solanesyl transferase

Author
item Hunter, Charles
item Saunders, Jonathan - University Of Florida
item Magallanes-lundback, Maria - University Of Florida
item Li, Qin-bao
item Tang, Hoang
item Christensen, Shawn
item Stinard, Phillip - University Of Florida
item Dellapenna, Dean - University Of Florida
item Koch, Karen - University Of Florida

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/20/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Maize white seedling 3 (w3) has served as a model albino-seedling mutant since its discovery in 1923. We show here that the w3 phenotype is caused by disruptions in homogentisate solanesyl transferase (HST), an enzyme that catalyzes the committed step in plastoquinone-9 (PQ9) biosynthesis. This reaction lies at the heart of a complex metabolic network of plastidial antioxidants, pigments, and phytohormones. Disruption of PQ9 biosynthesis has broad-ranging implications, from nutritional quality of grains to plant defense. Plastoquinone-9 is a redox cofactor required for electron transfer and proton translocation during photosynthesis. It also serves as an oxidant in the enzymatic desaturation of phytoene during the formation of carotenoids. Finally, plastoquinone-9 is the immediate precursor for plastochromanol-8 (PC8), a vitamin E analog with roles as a lipid-soluble antioxidant. As observed in corresponding Arabidopsis mutants, plastoquinone-9 deficiency resulted in albino seedlings defective in carotenoid biosynthesis at the level of phytoene desaturation, and accumulation of phytoene. Unlike in Arabidopsis, maize mutants showed a propensity for vivipary, typical of abscisic acid-deficient mutants, again resulting from carotenoid deficiency. In addition, the non-green seeds of maize provided a unique opportunity to examine the effects of plastoquinone deficiency on tocochromanol (tocopherol, tocotrienol, and PC8) accumulation in the absence of photo-oxidation. As in leaves, the absence of HST in seeds resulted in loss of PQ9, PC8, and carotenoids as well as the accumulation of phytoene. However, tocochromanol content in w3 kernels remained similar, supporting the hypothesis that HST’s influence on vitamin E levels was not due to a biosynthetic role per se, but rather to its protection of pigments (including chlorophyll and tocochromanols) in green tissues from photo-oxidative damage.