Following Vegetative to Embryonic Cellular Changes in Leaves of Arabidopsis thaliana Over-Expressing LEAFY COTYLEDON2.
Feeney, M., Frigerio, L., Cui, Y., and Menassa, R. (2013). "Following Vegetative to Embryonic Cellular Changes in Leaves of Arabidopsis thaliana Over-Expressing LEAFY COTYLEDON2.", Plant Physiology, 162(4), pp. 1881-1896. doi : 10.1104/pp.113.220996 Access to full text
Embryogenesis in flowering plants is controlled by a complex interplay of genetic, biochemical and physiological regulators. LEAFY COTYLEDON2 (LEC2) is among a small number of key transcriptional regulators that are known to play important roles in controlling major events during the maturation stage of embryogenesis, notably, the synthesis and accumulation of storage reserves. LEC2 over-expression causes vegetative tissues to change their developmental fate to an embryonic state however little information exists about the cellular changes that take place. We show that LEC2 alters leaf morphology and anatomy and causes embryogenic structures to form subcellularly in leaves of Arabidopsis thaliana. Chloroplasts accumulate more starch, the cytoplasm fills with oil bodies and lytic vacuoles (LVs) appear smaller in size and accumulate protein deposits. Since LEC2 is responsible for activating the synthesis of seed storage proteins (SSPs) during seed development, SSP accumulation was investigated in leaves. The major Arabidopsis SSP families were shown to accumulate within small leaf vacuoles. By exploiting the developmental and tissue specific localization of two tonoplast intrinsic protein (TIP) isoforms, the small leaf vacuoles were identified as protein storage vacuoles (PSVs). Confocal analyses of leaf vacuoles expressing fluorescently labeled TIP isoforms reveal an altered tonoplast morphology resembling an amalgamation of a LV and PSV. Results suggest that as the LV transitions to a PSV, the tonoplast remodels before the large vacuole lumen is replaced by smaller PSVs. Finally, using vegetative and seed markers to monitor the transition, we show that LEC2 induces a reprogramming of leaf development.
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