THE AXR2-1 MUTATION OF ARABIDOPSIS-THALIANA IS A GAIN-OF-FUNCTION MUTATION THAT DISRUPTS AN EARLY STEP IN AUXIN RESPONSE

Citation
C. Timpte et al., THE AXR2-1 MUTATION OF ARABIDOPSIS-THALIANA IS A GAIN-OF-FUNCTION MUTATION THAT DISRUPTS AN EARLY STEP IN AUXIN RESPONSE, Genetics, 138(4), 1994, pp. 1239-1249
Citations number
41
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
00166731
Volume
138
Issue
4
Year of publication
1994
Pages
1239 - 1249
Database
ISI
SICI code
0016-6731(1994)138:4<1239:TAMOAI>2.0.ZU;2-9
Abstract
The dominant axr2-1 mutation of Arabidopsis thaliana confers resistanc e to the plant hormones auxin, ethylene, and abscisic acid. In additio n, axr2-1 has pleiotropic effects on plant morphology which include gr avitropic defects in roots, hypocotyls and inflorescences of axr2-1 pl ants. Two genetic screens were conducted to isolate new mutations at t he AXR2 locus. First, axr2-1 pollen was gamma-irradiated, crossed onto wild-type plants, and the M(1) progeny screened for loss of the axr2- 1 phenotype. Large deletions of the axr2-1 region on chromosome 3 resu lted; however, none of these deletions appeared to be heritable. In th e second, M(2) seed obtained from axr2-1 gl-l plants was screened for reversion of the axr2-1 phenotype. One revertant line, axr2-r3, has a distinctive phenotype caused by a second mutation at the axr2 locus. T o learn more about the nature of the axr2-1 mutation, the effects of v arying the ratio of wild-type to mutant copies of the AXR2 gene were e xamined by comparing plants of the following genotypes: +/+, +/+/+, ax r2-1/axr2-1, axr2-1/+ and axr2-1/+/+. Additionally, accumulation of tr anscripts from the auxin-inducible SAUR-AC1 gene was examined to deter mine the response of wild-type and mutant plants to auxin. Wild-type s eedlings and mature plants accumulate transcripts with auxin treatment . In contrast, axr2-1 tissue does not accumulate SAUR-AC1 transcripts in response to auxin. Taken together, these results indicate that axr2 -1 is a neomorphic or hypermorphic mutation that disrupts an early ste p in an auxin response pathway.