Expressivity of tocopherol mutations in sunflower

Abstract

Influences of genetic background, ontogenesis and environment on tocopherol mutations in sunflower were estimated in this study. The content of α/β-tocopherols varied from 40/60 to 60/40% in seeds of different inbred lines containing the tph1 gene. The lines containing the tph2 gene ranged widely in α/γ-tocopherols, from 0/100 to 80/20%. A double mutation showed variability in different inbred lines in α/β/γ/δ-tocopherol contents from maximum expressivity of 0/0/60/40 to minimum 40/25/25/10%, due to incomplete expressivity of tph2. Seed maturation from 10 to 38 DAF influenced tocopherol composition in both normal and mutant genotypes by increasing the α-tocopherol content. The content varied from 81 to 97% in a normal genotype, from 33 to 50% in tph1 mutation and from 0 to 6% in tph2 mutation. Tocopherol mutations were shown to express their phenotype in different parts of a plant. All roots, hypocotyls, leaves, pollen and callus from the seeds, hypocotyls and leaves had normal, tph1, tph2 and double mutation tocopherol profiles depending on the genotype. The only exception was the absence of tph1 expressivity in the green tissue of the leaves. The experiment with day/night temperatures varying during seed development from 20/18 to 30/26°C showed an increased α-tocopherol content from 39 to 48% in tph1 mutation. Both a normal genotype (about 97% of α-tocopherol) and tph2 mutation (about 98% of γ-tocopherol) were constant in these two temperature regimes. Genetic background was the main factor that influenced the expressivity of tph2 in sunflower.

Expression of modified tocopherol content and profile in sunflower tissues

“…However, leaves contained either similar amounts of both gamma‐ and delta‐tocopherol (TS‐1) or predominantly gamma‐tocopherol (IAST‐4), which is explained on the basis of low expressivity of the tph1 mutation in leaves. This was described by Demurin et al 15 and also observed in the mutants with increased levels of beta‐tocopherol studied in the present research.…”

“…However, beta‐tocopherol levels in leaves were about three times lower than those found in seeds, suggesting a lower expression of the tph1 mutation in leaves. Demurin et al 15 described no expressivity of tph1 mutation in sunflower leaves in analyses conducted using thin layer chromatography. Since the beta‐tocopherol mutant LG‐15 analysed by Demurin et al 15 is allelic to T589,30 differences in beta‐tocopherol expression in leaves between the two studies might result from the more sensitive analytical technique used in the present research.…”

“…Simultaneous overexpression of HPT and gamma‐TMT resulted in an increase in total tocopherol content as well as almost complete methylation of gamma‐tocopherol to alpha‐tocopherol in both seeds and leaves 14. In sunflower, Demurin et al 15 studied the expressivity of seed tocopherol profile mutations in different parts of the plant. Although levels of individual tocopherols were not reported, the authors concluded that tph1 (increased beta‐tocopherol), tph2 (increased gamma‐tocopherol) and the double mutation tph1 tph2 (increased delta‐tocopherol) were expressed in roots, hypocotyls and pollen grains.…”

A rapid test for detection of tribenuron-methyl resistance in sunflower

“…Reduced growth in plants less tolerant to herbicides, after herbicide treatment, is considered to be a consequence of poor root growth and consequently decreased nutrient uptake (Soltani et al 2008). When testing herbicide tolerance one must consider that both environmental factors and the genetic basis of the genotypes receiving the resistance genes have large influence on the expression of herbicide resistance (Jocić et al 2011), especially bearing in mind that genetic background was found to influence the expressivities of some mutations in sunflower (Demurin et al 2006). Considering a wide range in plant growth response to stress conditions in sunflower in respect to different genetic background (Pereyra-Irujo et al 2008, Ahmad et al 2009), we tested several genotypes in order to identify universal treatment for detection of TBM resistance.…”