Abaxial epidermal cells of developing faba bean (Vicia faba) cotyledons are modified to a transfer cell morphology and function. In contrast, the adaxial epidermal cells do not form transfer cells but can be induced to do so when excised cotyledons are cultured on an agar medium. The first fenestrated layer of wall ingrowths is apparent within 24 h of cotyledon exposure to culture medium. The time course of wall ingrowth formation was examined further. By 2 h following cotyledon excision, a 350 nm thick wall was deposited evenly over the outer periclinal walls of adaxial epidermal cells and densities of cytoplasmic vesicles increased. After 3 h in culture, 10% of epidermal cells contained small projections of wall material on their outer periclinal walls. Thereafter, this percentage rose sharply and reached a maximum of 90% by 15 h. Continuous culture of cotyledons on a medium containing 6-methyl purine (an inhibitor of RNA synthesis) completely blocked wall ingrowth formation. In contrast, if exposure to 6-methyl purine was delayed for 1 h at the start of the culture period, the adaxial epidermal cells were found to contain small wall ingrowths. Treating cotyledons for 1 h with 6-methyl purine at 15 h following cotyledon excision halted further wall ingrowth development. We conclude that transfer cell induction is rapid and that signalling and early events leading to wall ingrowth formation depend upon gene expression. In addition, these gene products have a high turnover rate.

Somatic embryogenesis (SE) is a remarkable developmental process enabling nonzygotic plant cells to form embryos and ultimately, fertile plants. It is an expression of totipotency. This chapter initially considers the genotypic component and the progenitor stem cells where SE is induced to form the initial asymmetric division of the somatic embryogenesis program. These cells are part of a stem cell niche dependent on the surrounding cells. Recent evidence is discussed that before the SE pathway can be initiated a GA-modulated pathway that represses inappropriate embryogenesis needs to be derepressed. The current understanding of how stress and hormones can induce the activation of specific SE genes is examined. Important stress components are reactive oxygen species and the signalling of stress-related hormones. The action of the key developmental hormone auxin, and also cytokinin, in relation to developmental genes is considered and, based on current understanding, a model is presented for the mechanism of SE. While there are many SE applications in contemporary biotechnology, understanding the reprogramming process associated with SE remains an important question for developmental biology.