Regulation of lutein biosynthesis and prolamellar body formation in Arabidopsis.

Funct Plant Biol

ARC Centre of Excellence in Plant Energy Biology, School of Biochemistry and Molecular Biology, The Australian National University, Canberra, ACT 0200, Australia.

Published: August 2007

AI Article Synopsis

  • Carotenoids play a vital role in photosynthesis and the formation of prolamellar bodies in dark-grown seedlings, acting as precursors for plant hormones.
  • The study focuses on lutein biosynthesis regulation and how changes in carotenoid production affect the prolamellar body structure in etioplasts.
  • Analysis revealed that specific enzymes, CRTISO and epsilon-cyclase, are critical for lutein production, and targeted herbicide treatments confirmed that carotenoid accumulation directly impacts prolamellar body formation in lutein-deficient mutants.

Article Abstract

Carotenoids are critical for photosynthetic function in chloroplasts, and are essential for the formation of the prolamellar body in the etioplasts of dark-grown (etiolated) seedlings. They are also precursors for plant hormones in both types of plastids. Lutein is one of the most abundant carotenoids found in both plastids. In this study we examine the regulation of lutein biosynthesis and investigate the effect of perturbing carotenoid biosynthesis on the formation of the lattice-like membranous structure of etioplasts, the prolamellar body (PLB). Analysis of mRNA abundance in wildtype and lutein-deficient mutants, lut2 and ccr2, in response to light transitions and herbicide treatments demonstrated that the mRNA abundance of the carotenoid isomerase (CRTISO) and epsilon-cyclase (ϵLCY) can be rate limiting steps in lutein biosynthesis. We show that accumulation of tetra-cis-lycopene and all-trans-lycopene correlates with the abundance of mRNA of several carotenoid biosynthetic genes. Herbicide treatments that inhibit carotenoid biosynthetic enzymes in wildtype and ccr2 etiolated seedlings were used to demonstrate that the loss of the PLB in ccr2 mutants is a result of perturbations in carotenoid accumulation, not indirect secondary effects, as PLB formation could be restored in ccr2 mutants treated with norflurazon.

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Source
http://dx.doi.org/10.1071/FP07034DOI Listing

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