Plant Physiology Preview
Published on April 21, 2006; 10.1104/pp.105.076273
Received December 26, 2005
Returned for revision January 13, 2006
Accepted April 19, 2006
Inhibition of Brassinosteroid Biosynthesis by Either a dwarf4 Mutation or a Brassinosteroid Biosynthesis Inhibitor Rescues Defects in Tropic Responses of Hypocotyls in the Arabidopsis Mutant, non-phototropic hypocotyl 4
Daisuke Nakamoto , Akimitsu Ikeura , Tadao Asami , and Kotaro T. Yamamoto *
Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo, 060-0810 Japan
Division of Biological Sciences, Graduate School of Environmental Earth Science, Hokkaido University, Sapporo, 060-0810 Japan
Plant Functions Laboratory, RIKEN, Wako, 351-0198 Japan
Division of Biological Sciences, Graduate School of Science, Hokkaido University, Sapporo, 060-0810 Japan; Division of Biological Sciences, Graduate School of Environmental Earth Science, Hokkaido University, Sapporo, 060-0810 Japan
* Corresponding author; email: kty{at}sci.hokudai.ac.jp.
The nph4/arf7 mutant of Arabidopsis is insensitive to auxin and has defects in hypocotyl tropism, hook formation, differential growth of leaf and lateral root formation. To understand an auxin-signaling pathway through NPH4, we carried out screening of suppressor mutants of nph4-103, and obtained a recessive suppressor mutant, snp2 (suppressor of nph4), which was dwarf. snp2 had short hypocotyls in the dark condition, and dark green and round leaves, short petioles and more lateral shoots than the wild type in the light condition. The snp2 phenotypes were rescued by adding brassinolide to the growth medium in both light and dark conditions. Genetic mapping, sequence analysis and a complementation test indicated that snp2 was a weak allele of DWARF4 (DWF4) which functions in brassinosteroid (BR) biosynthesis. snp2, which was renamed dwf4-101, exhibited photo- and gravitropisms of hypocotyl similar to those of the wild type with a slightly faster response in gravitropism. dwf4-101 almost completely suppressed defects in both tropisms of nph4-103 hypocotyls, and completely suppressed hyponastic growth of nph4-103 leaves. Treatment with brassinazole, an inhibitor of BR biosynthesis, also partially rescued the tropic defects in nph4-103. Hypocotyls of nph4-103 were auxin insensitive, while hypocotyls of dwf4-101 were more sensitive than those of the wild type. dwf4-101 nph4-103 hypocotyls were as sensitive as those of dwf4-101. Auxin-inducibility of of the MSG2/IAA19 gene expression was reduced in nph4-103. mRNA level of MSG2/IAA19 was reduced in dwf4-101 and dwf4-101 nph4-103, but either mutant exhibited greater auxin inducibility of MSG2 than the wild type. Taken together, dwf4-101 was epistatic to nph4-103. These results strongly suggest that BR deficiency suppresses nph4-103 defects in tropistic responses of hypocotyls and differential growth of leaves, and that BR negatively regulates tropistic responses.
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