Characteristics and physiological causes of a precocious germination mutant of Chinese cabbage (Brassica rapa ssp. Pekinensis)
Precocious germination (PG) is the germination of immature seeds before desiccation. Development of Chinese cabbage seeds was divided into 10 distinct but contiguous stages. PG of seeds of the mutant occurred mainly during stages 5 to 8 of development, with either the radicle or cotyledons emerging from the testa. Maximum PG in situ was less than 20%, but when removed from the siliques and imbibed in water all mutant seeds germinated precociously. PG seeds could not tolerate desiccation while non-PG seeds of the mutant could, although their tolerance was less than that of wild-type seeds. Inhibition of ABA biosynthesis by fluridone induced more PG seeds, while high concentrations of ABA inhibited PG. Mutant seeds contained much higher ABA than wild-type seeds, but were about 10 times less sensitive to exogenous ABA. Therefore, reduced ABA-sensitivity, not ABA deficiency, was a likely physiological cause of PG. Removal of the testa facilitated embryo germination of both mutant and wild-type seeds, but was more effective for the wild-type. In some parts of the mutant seed testa, there was a reduction in secondary cell wall materials on the palisade cell walls, resulting in less mechanical restraint by the testa, and PG. Some developmental events were maintained within the naturally-occurring PG seeds following germination, but not in the PG seeds isolated and placed on water to induce germination. This was because of changes in the environment of the latter seeds. The decisive factors which maintained developmental events in the former seeds were ABA and nutrient supply, because when developing seeds were isolated and incubated in MS medium plus ABA, both developmental and germinative events coexisted in the induced PG seeds up to the time of establishment of the seedlings. This study shows there is a potential relationship between ABA and the accumulation of cell wall components in testa, the ABA transduction pathway, and the control of PG occurrence.