First published online July 18, 2002; 10.1104/pp.003780
Plant Physiol, August 2002, Vol. 129, pp. 1557-1567
Loss-of-Function Mutations in the Ethylene Receptor
ETR1 Cause Enhanced Sensitivity and Exaggerated Response to
Ethylene in Arabidopsis
Jesse D.
Cancel and
Paul B.
Larsen*
Department of Biochemistry, University of California, Riverside,
California 92521
Ethylene signaling in Arabidopsis begins at a family of five
ethylene receptors that regulate activity of a downstream
mitogen-activated protein kinase kinase kinase, CTR1. Triple and
quadruple loss-of-function ethylene receptor mutants display a
constitutive ethylene response phenotype, indicating they function as
negative regulators in this pathway. No ethylene-related phenotype has
been described for single loss-of-function receptor mutants, although
it was reported that etr1 loss-of-function mutants
display a growth defect limiting plant size. In actuality, this
apparent growth defect results from enhanced responsiveness to
ethylene; a phenotype manifested in all tissues tested. The phenotype
displayed by etr1 loss-of-function mutants was rescued
by treatment with an inhibitor of ethylene perception, indicating that
it is ethylene dependent. Identification of an ethylene-dependent
phenotype for a loss-of-function receptor mutant gave a unique
opportunity for genetic and biochemical analysis of upstream events in
ethylene signaling, including demonstration that the dominant
ethylene-insensitive phenotype of etr2-1 is partially
dependent on ETR1. This work demonstrates that
mutational loss of the ethylene receptor ETR1 alters responsiveness to
ethylene in Arabidopsis and that enhanced ethylene response in
Arabidopsis not only results in increased sensitivity but exaggeration
of response.
*
Corresponding author; e-mail paul.larsen{at}ucr.edu; fax
909-787-4434.
© 2002 American Society of Plant Physiologists
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