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First published online August 19, 2005; 10.1104/pp.105.064451

Plant Physiology 139:79-87 (2005)
© 2005 American Society of Plant Biologists

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BIOCHEMICAL PROCESSES AND MACROMOLECULAR STRUCTURES

Two FAD3 Desaturase Genes Control the Level of Linolenic Acid in Flax Seed

Patricia Vrinten, Zhiyuan Hu1, Mary-Ann Munchinsky, Gordon Rowland and Xiao Qiu*

Bioriginal Food and Science Corporation, Saskatoon, Saskatchewan, Canada S7N 0W9 (P.V., Z.H., M.-A.M., X.Q.); and Crop Development Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 0W9 (G.R.)

Industrial oil flax (Linum usitatissimum) and edible oil or solin flax differ markedly in seed linolenic acid levels. Despite the economic importance of low-linolenic-acid or solin flax, the molecular mechanism underlying this trait has not been established. Two independently inherited genes control the low-linolenic-acid trait in flax. Here, we identified two genes, LuFAD3A and LuFAD3B that encode microsomal desaturases capable of desaturating linoleic acid. The deduced proteins encoded by these genes shared 95.4% identity. In the low-linolenic-acid line solin 593-708, both LuFAD3A and LuFAD3B carry point mutations that produce premature stop codons. Expression of these genes in yeast (Saccharomyces cerevisiae) demonstrated that, while the wild-type proteins were capable of desaturating linoleic acid, the truncated proteins were inactive. Furthermore, the low-linolenic-acid phenotype in flax was complemented by transformation with a wild-type gene. Codominant DNA markers were developed to distinguish between null and wild-type alleles of both genes, and linolenic acid levels cosegregated with genotypes, providing further proof that LuFAD3A and LuFAD3B are the major genes controlling linolenic acid levels in flax. The level of LuFAD3 transcripts in seeds peaked at about 20 d after flowering, and transcripts were not detectable in leaf, root, or stem tissue. A dramatic reduction in transcript levels of both genes occurred in the low-linolenic-acid solin line, which was likely due to nonsense-mediated decay.


1 Present address: Lineberger Comprehensive Cancer Center, CB# 7295, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.064451.

* Corresponding author; e-mail xqiu{at}bioriginal.com; fax 306–975–4839.

Received April 20, 2005; returned for revision July 8, 2005; accepted July 11, 2005.




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