ashi@nuagr1.agr.nagoya-u.ac.jp
As the result of Rice Genome Research, we can
available many tools including molecular markers, genomic libraries, sequences
data, many mutants produced by tag lines, microarray and proteome system. These
progresses give us many chances to approach to science and breeding. Here we
introduce rice genomics application to our research, study of Gibberellin (GA)
biosynthetic, signal transduction pathway (1,2 and 3). And
also we show the rice genomics application to the molecular breeding (4
and 5).
We has been collected and maintained many rice mutants including dwarf and slender
mutants. Dwarf mutants in plants are crucial for elucidating regulatory mechanisms
for plant growth, development and response to plant hormones. We have screened
GA-sensitive and insensitive rice mutants. We have cloned several genes associated
with GA biosynthesis and 3 genes associated with GA signal transduction by using
the rice genomics.
A rice dwarf mutant Daikoku carrying the d1 gene is not only short, but
also has broad, dark green leaves, compact panicles, and short, round grains.
These phenotypes are all controlled by a recessive allele (d1) of the
rice Dwarf1 (D1). The mutant was characterized as Gibberellin
(GA)-insensitive, because no production of alpha-amylase in the d1 mutant
was detectable by application of GA3. For clarifying the molecular mechanisms
of GA signal transduction, the rice Dwarf 1 (D1) gene was isolated
by a map-based cloning strategy. (1, 2).
The rice slender mutant (slr1-1) is caused by a single recessive
mutation and results in a constitutive gibberellin (GA) response phenotype.
The mutant elongates as if saturated with GAs. Some results indicate that the
product of the SLR1 gene is an intermediate of the GA signal transduction
pathway and slr1-1 mutant is caused by a loss-of-function mutation of
the SLR1 gene, which is an ortholog of GAI, RGA, RHT,
and D8 which are associate with GA signal (3).
The gid1 (gibberellin insensitive dwarf1) mutant shows severe
dwarf phenotype similar to that of the null allele of d18, which is a deficient
mutant of GA biosynthesis. In gid1seedlings, however, endogenous GA1
content was almost 120 times higher than that in wild plant and the application
of exogenous GA3 did not restore phenotype. These results indicated that gid1
is defective in the perception to GA, and the GID1 gene may encode a
positive regulator of GA signaling. Recently, we succeeded to clone the gid1
gene with Yue-ie Caroline Hsing lab. collaboration, Academia Sinica.
Analyzing the function of these genes, epistatic interaction and biochemistry
approach guides us the outline of GA signal transduction. And now we can control
the plant height and plant type with modification of these plant hormone genes.
(1).Proc.
Natl. Acad. Sci. USA., (1999)
96, 10284-10289.
(2).Proc. Natl. Acad. Sci., USA., (2000) 97,
11638-11643.
(3).Plant Cell, (2001)
13, 999-1010.
(4).Plant Cell, (2000) 12,
1591-1605.
(5).Plant Cell (2000) 12.
2473-2483