A mutational approach to the study of seed development in maize.

The maize seed comprises two major compartments, the embryo and the endosperm, both originating from the double fertilization event. The embryogenetic process allows the formation of a well-differentiated embryonic axis, surrounded by a single massive cotyledon, the scutellum. The mature endosperm constitutes the bulk of the seed and comprises specific regions containing reserve proteins, complex carbohydrates, and oils.

Light-Dependent Spatial and Temporal Expression of Pigment Regulatory Genes in Developing Maize Seeds.

Both light and developmental stimuli are directly involved in the regulation of plant gene expression. In maize, activation of the anthocyanin pathway represents an excellent model system for studying the interactions between an external factor, such as light, and internal factors that regulate plant and seed development. By analyzing in detail the aleurone and pericarp seed layers, different developmental windows for light have been found in the two tissues[mdash]the former in the advanced stages of development and the latter in the early stages of seed development.

Programmed cell death during embryogenesis in maize.

Programmed cell death (PCD) in plants is considered an integral part of development. Evidence of DNA fragmentation, occurring at specific sites and times during embryo formation in maize (Zea mays L.), was obtained using terminal deoxyribonucleotidyl transferase-mediated dUTP-fluorescein nick end labelling (TUNEL) and by genomic DNA ladder detection.

Mutations in two independent genes lead to suppression of the shoot apical meristem in maize.

The shoot apical meristem (SAM), initially formed during embryogenesis, gives rise to the aboveground portion of the maize (Zea mays) plant. The shootless phenotype (sml) described here is caused by disruption of SAM formation due to the synergistic interaction of mutations at two genetic loci. Seedlings must be homozygous for both sml (shootmeristemless), and the unlinked dgr (distorted growth) loci for a SAM-less phenotype to occur.