The relationship between ethylene binding and dominant insensitivity conferred by mutant forms of the ETR1 ethylene receptor
Ethylene responses in Arabidopsis are mediated by a small family of receptors, including the ETR1 gene product. Specific mutations in the N-terminal ethylene-binding domain of any family member lead to dominant ethylene insensitivity. To investigate the mechanism of ethylene insensitivity, the authors examined the effects of mutations on the ethylene-binding activity of the ETR1 protein expressed in yeast. The etr1-1 and etr1-4 mutations completely eliminated ethylene binding, while the etr1-3 mutation severely reduced binding. Additional site-directed mutations that disrupted ethylene binding in yeast also conferred dominant ethylene insensitivity when the mutated genes were transferred into wild-type Arabidopsis plants. By contrast, the etr1-2 mutation did not disrupt ethylene binding in yeast. These results indicate that dominant ethylene insensitivity may be conferred by mutations that disrupt ethylene binding or that uncouple ethylene binding from signal output by the receptor. Increased dosage of wild-type alleles in triploid lines led to the partial recovery of ethylene sensitivity, indicating that dominant ethylene insensitivity may involve either interactions between wild-type and mutant receptors or competition between mutant and wild-type receptors for downstream effectors.
- Research Organization:
- Univ. of Wisconsin, Madison, WI (US)
- Sponsoring Organization:
- National Science Foundation (NSF); USDOE
- DOE Contract Number:
- FG02-91ER20029
- OSTI ID:
- 20006208
- Journal Information:
- Plant Physiology (Bethesda), Vol. 121, Issue 1; Other Information: PBD: Sep 1999; ISSN 0032-0889
- Country of Publication:
- United States
- Language:
- English
Similar Records
Ethylene-binding sites generated in yeast expressing the Arabidopsis ETR1 gene
A strong constitutive ethylene-response phenotype conferred on Arabidopsis plants containing null mutations in the ethylene receptors ETR1 and ERS1