Reference "slender rice, a constitutive gibberellin response mutant, is caused by a null mutation of the SLR1 gene, an ortholog of the height-regulating gene GAI/RGA/RHT/D8"

Reference ID

7060

Title

slender rice, a constitutive gibberellin response mutant, is caused by a null mutation of the SLR1 gene, an ortholog of the height-regulating gene GAI/RGA/RHT/D8

Source

The Plant cell, 2001, vol. 13, pp. 999-1010

Authors (8)

Ikeda-A	Ueguchi-Tanaka-M
Sonoda-Y	Kitano-H
Koshioka-M	Futsuhara-Y
Matsuoka-M	Yamaguchi-J

Abstract

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. In this mutant, (1) elongation was
unaffected by an inhibitor of GA biosynthesis, (2) GA-inducible alpha-amylase
was produced by the aleurone layers without gibberellic acid application, and
(3) endogenous GA content was lower than in the wild-type plant. These results
indicate that the product of the SLR1 gene is an intermediate of the GA signal
transduction pathway. SLR1 maps to OsGAI in rice and has significant homology
with height-regulating genes, such as RHT-1Da in wheat, D8 in maize, and GAI and
RGA in Arabidopsis. The GAI gene family is likely to encode transcriptional
factors belonging to the GRAS gene superfamily. DNA sequence analysis revealed
that the slr1-1 mutation is a single basepair deletion of the nuclear
localization signal domain, resulting in a frameshift mutation that abolishes
protein production. Furthermore, introduction of a 6-kb genomic DNA fragment
containing the wild-type SLR1 gene into the slr1-1 mutant restored GA
sensitivity to normal. These results indicate that the 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. We also succeeded in producing GA-insensitive dwarf rice by
transforming wild-type rice with a modified SLR1 gene construct that has a 17-
amino acid deletion affecting the DELLA region. Thus, we demonstrate opposite GA
response phenotypes depending on the type of mutations in SLR1.