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Embryogenesis in higher plants can be divided conceptually into two distinct phases. Early in embryogenesis, during the morphogenesis
phase, the basic body plan of the plant is established with regional specification of apical–basal and radial domains from
which morphological structures derive, fixation of polarity from specification of the shoot-root axis, and formation of embryonic
tissue and organ systems (1–3). The morphogenesis phase is followed temporally by the maturation phase, although the two phases can overlap (4, 5). During the maturation phase, embryo cell-division rates decline markedly, embryo cells acquire the ability to withstand
desiccation, and embryo cell growth occurs, with the accumulation of storage reserves that comprise lipids and proteins in
Arabidopsis (6, 7). At the end of the maturation phase, the embryo becomes quiescent metabolically as the seed desiccates.
The maturation phase can be viewed as an interruption of an ancestral life cycle, as occurs in lower plants, in which there
are no periods of maturation or dormancy separating the end of embryogenesis and the beginning of postembryonic development
(4). Evolution of this unique mode of embryogenesis has enabled higher plants to make seeds. The ability to make seeds has provided
tremendous selective advantages that, in part, account for the success of the angiosperms (8, 9). Little is known at a mechanistic level about the processes by which the maturation phase has been integrated into the higher
plant life cycle.
LEAFY COTYLEDON2 (LEC2), along with ABA INSENSITIVE3 (ABI3), and FUSCA3 (FUS3), have been implicated to be major regulators
of the maturation phase (reviewed in ref. 5). The LEC2 protein contains a DNA-binding B3 domain that is most closely related to that of FUS3 and ABI3 (10–12). The lec2 mutation causes localized defects in embryo filling, seed protein accumulation, and desiccation tolerance (12, 13). LEC2 expression is normally limited primarily to seed development, although LEC2 RNA may be present at very low levels at other stages of the life cycle (12). Ectopic expression of LEC2 causes accumulation of seed storage lipids and proteins in vegetative organs (ref. 14, and S.L.S., S. L. Paula, L. W. Kwong, J. E. Meuser, J. Pelletier, R.L.F., R.B.G., and J.J.H., unpublished work). The function
of LEC2 is not limited to the maturation phase. The lec2 mutation causes defects during the morphogenesis phase, and ectopic LEC2 expression induces somatic embryo formation from vegetative cells (12, 13). Furthermore, the lec2 mutation severely compromises the ability of Arabidopsis explants to form somatic embryos (15). These observations suggest that LEC2 plays several roles during embryogenesis, indicating that it is a central regulator
of embryo development.
To gain insight into the role of LEC2 in embryogenesis, we have identified genes regulated by the LEC2 transcription factor.
We show that a subset of genes activated by LEC2 is expressed predominantly during the maturation phase, and several have
known roles in maturation processes. Several of these maturation genes are also expressed early in embryogenesis. We also
show that all of these genes possess a common DNA motif that is bound by LEC2, providing strong evidence that these genes
are regulated directly by LEC2. The identity of LEC2 target genes suggests a link between the ability of LEC2 to induce maturation
processes and somatic embryogenesis.
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