REVERSION-TO-ETHYLENE-SENSITIVITY1: A Novel Regulator of Ethylene Receptor Function in Arabidopsis thaliana

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2006-11-25

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Abstract

Ethylene is a plant hormone that has profound effects on plant growth and development. Genetic analysis has been central in the elucidation of the ethylene-signaling pathway, made possible through the isolation of ethylene-response mutants in Arabidopsis. This thesis focuses on elucidating the function of the Arabidopsis REVERSION-TO-ETHYLENE-SENSITIVITY1 (RTE1) locus, which was identified in a genetic screen for suppressors of the ethylene-insensitive receptor mutant etr1-2.

The RTE1 gene was cloned by positional cloning and found to encode a novel integral membrane protein with homologs in plants and animals, but with no known molecular function. Our studies show that RTE1 is a negative regulator of the ethylene-response pathway, specifically acting as a positive regulator of the ETR1 ethylene receptor. Loss-of-function mutations in the RTE1 gene suppress the etr1-2 ethylene-insensitive phenotype, and genetic analysis suggests that loss of RTE1 results in a largely non-functional ETR1-2 mutant receptor. Similarly, wild-type ETR1 function appears to be greatly reduced in the absence of RTE1. Overexpression of the RTE1 gene confers weak ethylene insensitivity that is largely dependent on ETR1. rte1 mutations do not appear to affect the other four ethylene receptors of Arabidopsis, indicating that RTE1 specifically regulates ETR1. Sequence analysis revealed regions of conserved cysteine and histidine residues, and one rte1 loss-of-function mutant contains a point mutation at Cys161. Since such residues are common in metal binding proteins, we explored the possibility that RTE1 may be involved in facilitating the binding of an essential copper cofactor to the ETR1 receptor. However, experimental evidence suggests that this is not the likely role of RTE1.

Interestingly, rte1 was unable to suppress the ethylene insensitive mutant etr1-1, indicating that the differences between etr1-2 and etr1-1 may hold a clue as to how RTE1 regulates ETR1. A suppression analysis of eleven additional etr1 insensitive mutants suggests that RTE1 plays a role in regulating signaling by the transmitter domain of ETR1. A possible role for RTE homologs in non-plant systems is also discussed, although more work is required to elucidate a detailed biochemical model for RTE1 action.

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