Search

Bisporic embryo sacs contain nuclei derived from two members of a megaspore tetrad whereas tetrasporic embryo sacs contain nuclei derived from all four members of a tetrad. Megaspores from the same tetrad are less genetically similar than are megaspores from different tetrads. Therefore, cells derived from different megaspores in bisporic and tetrasporic embryo sacs are expected to compete with each other rather than cooperate. The tacit assumption of the plant embryological literature that bisporic and tetrasporic embryo sacs function as integrated organisms is demonstrably false, both theoretically and empirically. This competition within embryo sacs can be expressed as the formation of eggs by descendants of more than one megaspore or by the suppression of the descendants of all but one megaspore. Both phenomena have evolved multiple times. In contrast, all nuclei of monosporic female gametophytes are genetically identical. Consequently, monosporic development is predicted to be more evolutionarily stable than bisporic or tetrasporic development. The triploid endosperm produced by most monosporic gametophytes was probably derived from an ancestrally diploid endosperm and has been considered a key adaptation of the most successful lineages of flowering plants. The greater weight given to the doubled maternal genome in triploid endosperm may have facilitated a more efficient distribution of resources among a mother’s seeds because it reduced the influence of competition for maternal resources among unrelated paternal genomes of endosperm.

The plant life cycle alternates between two genetically active generations: the diploid sporophyte and the haploid gametophyte. In angiosperms the gametophytes are sexually dimorphic and consist of only a few cells. The female gametophyte, or embryo sac, is comprised of four cell types: two synergids, an egg cell, a central cell, and a variable number of antipodal cells. In some species the antipodal cells are indistinct and fail to proliferate, so many aspects of antipodal cell function and development have been unclear. In maize and many other grasses, the antipodal cells proliferate to produce a highly distinct cluster at the chalazal end of the embryo sac that persists at the apex of the endosperm after fertilization. The antipodal cells are a site of auxin accumulation in the maize embryo sac. Analysis of different families of genes involved in auxin biosynthesis, distribution, and signaling for expression in the embryo sac demonstrates that all steps are expressed within the embryo sac. In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells. Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells. The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells.

The plant life cycle alternates between two genetically active generations: the diploid sporophyte and the haploid gametophyte. In angiosperms the gametophytes are sexually dimorphic and consist of only a few cells. The female gametophyte, or embryo sac, is comprised of four cell types: two synergids, an egg cell, a central cell, and a variable number of antipodal cells. In some species the antipodal cells are indistinct and fail to proliferate, so many aspects of antipodal cell function and development have been unclear. In maize and many other grasses, the antipodal cells proliferate to produce a highly distinct cluster at the chalazal end of the embryo sac that persists at the apex of the endosperm after fertilization. The antipodal cells are a site of auxin accumulation in the maize embryo sac. Analysis of different families of genes involved in auxin biosynthesis, distribution, and signaling for expression in the embryo sac demonstrates that all steps are expressed within the embryo sac. In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells. Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells. The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells. [ABSTRACT FROM AUTHOR]