Abstract
The haploid female gametophyte (embryo sac) is an essential reproductive unit of flowering plants, usually comprising four specialized cell types, including the female gametes (egg cell and central cell). The differentiation of these cells relies on spatial signals which pattern the gametophyte along a proximal-distal axis, but the molecular and genetic mechanisms by which cell identities are determined in the embryo sac have long been a mystery. Recent identification of key genes for cell fate specification and their relationship to hormonal signaling pathways that act on positional cues has provided new insights into these processes. A model for differentiation can be devised with egg cell fate as a default state of the female gametophyte and with other cell types specified by the action of spatially regulated factors. Cell-to-cell communication within the gametophyte is also important for maintaining cell identity as well as facilitating fertilization of the female gametes by the male gametes (sperm cells).
Highlights
The flowering plants that dominate our landscapes and agriculture alternate between a diploid sporophytic stage, which constitutes the main body of the plant, and a reduced, haploid gametophytic stage contained within the male and female floral organs
Fusion of male and female gametes occurs during double fertilization, after the sperm cells are delivered to the embryo sac by the pollen tube
female gametophyte (FG) development in flowering plants begins after meiosis, when one of four haploid daughter cells develops into the functional megaspore (FM)
Summary
The flowering plants that dominate our landscapes and agriculture alternate between a diploid sporophytic stage, which constitutes the main body of the plant, and a reduced, haploid gametophytic stage contained within the male and female floral organs. Ectopic expression of the auxin biosynthesis YUCCA genes appears to shift micropylar cell fates toward the chalazal end of the gametophyte, conferring synergid and egg cell marker expression onto the central cell and antipodal cells[14]. Cki[1] mutants show loss of central cell and antipodal identities and expansion of egg cell and, in some cases, synergid attributes, suggesting that CKI1 suppresses micropylar cell fates[29,30,31].
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