Early Events in Maize Seed Development

Abstract

charge ( 12). This is contrasted with quiescence which is caused by external factors, e.g. anoxia, water drought. Without the onset and maintenance of dormancy there is the continued development of the embryo, otherwise referred to as 'vivipary' or 'preharvest sprouting.' Our current understanding of the onset of dormancy in maize seed is principally based on the characterization of several independent genes which control vivipary (7)(8)(9)(10)(11)13 possible temperature-dependent effects with material that was pollinated over a several-day period. At the appropriate DAP4, the husk leaves were cut and pulled back to expose the developing seeds. After the remaining silks were removed, solutions were sprayed or painted on the seeds. Fluridone (1-methyl-3-phenyl-5-[3-trifluoromethyl)phenyl]-4-( IH)-pyridinone) was applied in 1% (v,v) acetone-water. ABA was applied as a I mm aqueous solution. The husk leaves were gently refolded over the seeds, and the ear was rebagged, dated, and labeled. In all experiments reported here, the seeds were allowed to fully mature in the field until the stems and leaves had died, or at about 45 to 50 DAP.From five to ten ears were used for each treatment date. Ears which were damaged by insects or diseases were not used. After harvesting the ears, the seeds were removed from the ear and seeds separated from viviparous ones. Figure I shows the typical range of response seen with fluridone-treated seeds. RESULTSFluridone and other pyridinone, and pyridazinone, compounds, are known to inhibit the desaturation reactions converting phytoene to phytofluene in algae and in higher plants (1,6). Seeds treated with fluridone at 5 to 7 DAP appeared white at maturity whereas those seeds treated later in relation to the pollination date appeared increasingly yellow (Fig. 1)

Truncation of LEAFY COTYLEDON1 Protein Is Required for Asexual Reproduction in Kalanchoë daigremontiana

“…The inhibition of de novo ABA biosynthesis by fluridone in the newly formed leaves of these plants caused a complete break of leaf embryo dormancy and induced their "germination." Our results are in agreement with two other reports, which showed that the applications of fluridone to developing embryos, before the increase of endogenous ABA levels, prevented both ABA accumulation and development of embryo dormancy (Fong et al, 1983;White et al, 2000). On the other hand, none of the exogenous ABA applications could aggravate the transgenic dormant seed-like phenotype, nor did they affect normal wildtype leaf embryo development (data not shown).…”

“…7E, L2) of the same plant. This is consistent with the fluridone effect on seed embryo dormancy breaking prior to ABA accumulation (Fong et al, 1983;Le Page-Degivry et al, 1990;Yoshioka et al, 1998). While fluridone is known to have multiple pleiotropic effects on the plant, our results show that fluridone can restore normal plantlet development, likely due to systemic ABA biosynthesis inhibition prior to its accumulation.…”

“…In fact, the ABA-deficient maize mutant kernels are viviparous and precociously germinate in spite of a large contribution of ABA from the maternal plant (White et al, 2000). These results have led to the supposition that a threshold level of ABA at the appropriate time is required to block viviparous development (Fong et al, 1983;White et al, 2000).…”

“…Interestingly, ABA applications failed to aggravate the transgenic dormant seed-like phenotype and did not affect normal wild-type plantlet development (data not shown). One explanation for this result is that the window of developmental time during which ABA can impose dormancy is narrow and was missed during our experiments (Fong et al, 1983;White et al, 2000).…”

“…In addition, in many instances, seed dormancy can be released by applying fluridone, an inhibitor of carotenoid synthesis that causes a decrease in endogenous ABA levels (Yoshioka et al, 1998;Grappin et al, 2000). Application of fluridone to the embryos prior to ABA accumulation is proven to reduce ABA levels and prevent onset of embryo dormancy (Fong et al, 1983;Le PageDegivry et al, 1990;Yoshioka et al, 1998). We have used fluridone to prevent ABA accumulation in dormant seed-like transgenic leaf embryos and investigated whether reducing ABA could break the dormancy in these defective leaf embryos.…”