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The Relationship between Ethylene Binding and Dominant Insensitivity Conferred by Mutant Forms of the ETR1 Ethylene Receptor1

Anne E. Hall, Qianhong Grace Chen, Jennifer L. Findell, G. Eric Schaller, and Anthony B. Bleecker*

Department of Botany, University of Wisconsin, Madison, Wisconsin 53706 (A.E.H., Q.G.C., A.B.B.); and Department of Biochemistry and Molecular Biology, University of New Hampshire, Durham, New Hampshire 03824 (J.L.F., G.E.S.)

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, we 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.

1   This work was supported by the National Science Foundation (grant no. MCB-9603679 to G.E.S. and grant no. MCB-9513463 to A.B.B.), the HATCH project (grant no. 386 to G.E.S.), the Department of Energy (grant no. DE-FG02-91ER20029 to A.B.B.), and the Department of Energy-National Science Foundation-U.S. Department of Agriculture Collaborative Research in Plant Biology Program (grant no. BIR92-20331 to support A.E.H.).
*   Corresponding author; e-mail Bleecker{at}facstaff.wisc.edu; fax 608-262-7509.

Plant Physiol. (1999) 121: 291-300
Copyright Clearance Center:   0032-0889/99/121//10
© 1999 American Society of Plant Physiologists




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