Experiments were performed to assess regulatory factors governing maize
embryo maturation and vivipary. Both visual and molecular markers of embryo
development were used to examine the roles of the hormones abscisic acid (ABA)
and gibberellins (GAs), as well as water stress in governing transit from early
embryogeny to maturation-phase development. A differential screen identified
cDNAs whose expression is impaired in maize viviparous mutants which fail to
undergo maturation and instead precociously germinate. The cDNAs isolated in this
screen absolutely required both ABA and the Viviparousl (Vpl) gene product for
expression both in vivo and in vitro. Two novel clones were isolated: a maize
homologue of the wheat metallothionein gene E[subscript]c and a second clone which may
encode a novel seed storage protein of maize. In a separate screen, a maize cDNA
encoding a Lea group 3 protein was isolated. Like many maturation-associated
genes, maize Lea 3 was shown to ABA-inducible but is also expressed in response
to water stress in the absence of ABA or the Vp 1 gene.
We examined whether gibberellins might also be a factor modulating
precocious germination. Gibberellin inhibitors applied to cultured wildtype embryos
suppressed precocious germination and enhanced anthocyanin accumulation in a
developmentally specific manner. These behaviors mimicked the effect of ABA and
they were reversed by the addition of exogenous GA���. Vivipary in vivo resulting
from diminished ABA levels could be suppressed by either chemical or genetic
reduction of GA levels in immature kernels and resulted in desiccation-tolerant seed.
In contrast, reduction of endogenous gibberellins did not suppress vivipary of the
ABA-insensitive mutant vp1. Temporal analysis of gibberellin accumulation in
developing kernels revealed the accumulation of two bioactive species (GA��� and
GA���) during a developmental window just prior to peak ABA levels. It is suggested
that these species stimulate a developmental program leading to vivipary in the
absence of sufficient levels of ABA and that reduction of GA levels reestablishes a
hormone balance appropriate for suppression of germination and induction of
maturation in ABA-deficient kernels. The failure to suppress vivipary via reduction
of GA levels in the ABA-insensitive mutant vp1 suggests that the wildtype gene
product functions downstream of the sites of GA and ABA action in regulation of
maturation versus germination. / Graduation date: 1995
| Identifer | oai:union.ndltd.org:ORGSU/oai:ir.library.oregonstate.edu:1957/35014 |
| Date | 13 January 1995 |
| Creators | White, Constance N. |
| Contributors | Rivin, Carol J. |
| Source Sets | Oregon State University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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