| Research Abstract |
It is thought that seed desiccation tolerance is induced by maternally produced abscisic acid (ABA) through accumulation of Lea proteins of which the expression is controlled by ABI3/VP1 factor, a mediator of ABA signal transduction. However, the molecular mechanisms of the ABA-induced seed desiccation tolerance remains to be clarified, because it is very difficult to collect zygotic embryos at the same developmental stages. Then, I had investigated to clarify the mechanisms using carrot somatic embryos, because we can easily collect many embryos at the same developmental stages. At first, I clarified that somatic embryos acquire strong desiccation tolerance by exgenously appied ABA.Next, I had cloned a carrot gene (C-ABI3) homologous to ABI3/VP1 gene and examined the expression pattern. C-ABI3 showed embryo-specific expression in both somatic and zygotic embryos. The expression in carrot seeds was observed prior to the transient increase of endogenous ABA in the seeds. Furthermore, I had produced transgenic carrot plants and cultured cells in which C-ABI3 was expressed in the leaves or cells. Using these plants and cultured cells treated with ABA, I had examined the expression pattern of carrot ECP genes, the expression being embryo-specific and ABA-inducible and belonging to Lea gene family. The results showed that the expression of some ECP genes was observed in ABA-treated leaves and cells, but not in ABA non-treated ones and non-transformed ones irrespective of ABA treatment. Moreover, ABA-treated transgenic cultured cells showed clearly, desiccation tolerance. These results indicate that C-ABI3 is an embryo-specific transcription factor and that seed desiccation tolerance is acquired by ABA-inducibIe expression of ECP genes and accumulation of ECP proteins which are controlled by C-ABI3 factor as a mediator of ABA signal transduciton.
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