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THE PLANT CELL, Vol 8, Issue 4 659-671, Copyright © 1996 by American Society of Plant Biologists
A Dissociation Insertion Causes a Semidominant Mutation That Increases Expression of TINY, an Arabidopsis Gene Related to APETALA2
K. Wilson, D. Long, J. Swinburne and G. Coupland
Department of Molecular Genetics, John Innes Centre, Colney, Norwich NR4 7UJ, United Kingdom
A novel transposon-tagging strategy designed to recover dominant
gain-of-function alleles was performed with Arabidopsis by using a
Dissociation element with a cauliflower mosaic virus 35S promoter
transcribing outward over one terminus. Lines containing transposed copies
of this transposon were screened for mutants, and a semidominant mutation
affecting plant height, hypocotyl elongation, and fertility was recovered.
The pleiotropic effects of this mutation appear to result from a general
reduction in cell expansion, and some of the effects are similar to those
caused by supplying exogenous ethylene or cytokinin to wild-type seedlings.
In addition, the arrangement of cells in some organs, such as the etiolated
hypocotyl, is disorganized. The mutation was called tiny, and the affected
gene was cloned by first using transposon sequences to isolate the mutant
allele. The predicted protein product of the TINY gene shows strong
homology with the DNA binding domain of a recently identified class of
plant transcription factors. This domain, called the APETALA2 domain, was
initially identified as a duplicated region within the APETALA2 gene of
Arabidopsis and then as a conserved region between APETALA2 and the
ethylene responsive element binding proteins of tobacco. In the mutant
allele, the Dissociation element is inserted in the untranslated leader of
the TINY gene, 35 bp from the ATG, and the mutant contains a novel
transcript that initiates from the cauliflower mosaic virus 35S promoter
within the transposon. This transcript is present in greater abundance than
the wild-type TINY transcript; therefore, the semidominant tiny mutation
most likely results from increased, or ectopic, expression of the gene.
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