Ethylene is a simple phytohormone known to be involved with many processes crucial to plant development, including fruit ripening and tissue senescence. In an effort to identify novel factors involved in ethylene signaling, a screen was conducted for lines that display an enhanced ethylene response (eer). This resulted in isolation of fer-2, which demonstrates increased ethylene sensitivity. Map-based cloning revealed that fer-2 results from T-DNA insertion in the receptor-like kinase FERONIA (FER), which is involved with pollen tube growth. Genetic analysis indicates that fer-2 is capable of signaling in the absence of EIN2, supporting a model for EIN2-independent ethylene response mechanisms. fer-2 also displays decreased sensitivity to brassinosteroid (BR) signaling in etiolated hypocotyls, indicating that FER is required for proper BR response in dark-grown seedlings. This has led to development of a model where signaling by ethylene and low concentrations of BR in etiolated hypocotyls is finely balanced, with ethylene inhibiting growth and BR promoting growth in a FER-dependent manner.
A second screen was conducted for mutants that are weakly insensitive to ethylene by isolation of suppressors that restore wt response to ethylene in eer5-1. This led to identification of a new allele of ERS1, ers1-4, which results in reduced ethylene sensitivity in a semi-dominant manner. The reduction in sensitivity in the suppressor, ers1-4;eer5-1, is correlated with restored expression of AtEBP, supporting a role for AtEBP as a negative regulator of ethylene response. Sequencing of ers1-4 revealed an amino acid subsitution in the third transmembrane domain of ERS1, similar to the previously characterized etr1-2. Unlike ers1-4, etr1-2 does not strongly suppress eer5-1 and does not greatly affect expression of AtEBP, indicating a divergence of functions between the receptors. Furthermore, loss of RTE1 does not have as strong of an effect in ers1-4 as it does in etr1-2. Additional genetic analysis indicates that while signaling by ers1-4 is largely independent of ETR1, EIN2 is required for effective signaling. The evidence suggests that while there may be some crossover, ETR1 and ERS1 are capable of using distinct mechanisms to dampen the ethylene response, with ERS1 acting through AtEBP and ETR1acting through RTE1.