UC Riverside

Ethylene is a simple plant hormone involved in fruit ripening, tissue senescence, germination and pathogen response. The characteristic triple response phenotype in Arabidopsis has facilitated screening for mutants that affect ethylene signaling. A chemical library screen for altered ethylene response downstream of the ethylene receptors, led to the discovery of a new anti-auxinic compound, Pamoic Acid (PA), possibly linking the two phytohormones. Col-0 wild type etiolated seedlings grown in the presence of PA and saturating amounts of ethylene display longer hypocotyls and roots and are unhooked, which originally suggested a role for PA in disrupting the ethylene signaling response. Further phenotypic studies revealed that PA behaves similarly to a known anti-auxin p-Chlorophenoxyisobutyric acid (PCIB). Pamoic Acid has a chemical structure similar to two molecules of the synthetic auxin Naphthaleneacetic acid (NAA) and presumably can interfere with auxin signaling by binding to auxin receptors and prevent AUX/IAA turnover. This suggests that PA has an effect on normal ethylene response through alteration of auxin signaling, thus explaining the previously reported synergy between the two phytohormones.

A different screening method was employed to isolate mutants with an increased response to ethylene in an effort to isolate factors that function to reset the pathway following a signal. A new allele of pmr6 was identified as having an aberrant ethylene response phenotype. PMR6, which encodes a putative pectate lyase, is presumed to be involved in regulation of aspects of ethylene response by control of cell wall degradation. Further characterization revealed that loss of PMR6 led to severe reduction in capability to form an apical hook suggesting a role in this ethylene-dependent phenomenon. Interestingly, this mutant does not follow the same gene expression pattern as other eer mutants, where failure to induce a subset of genes, including AtEBP, is observed following ethylene treatment. pmr6-6 is sensitive to feeding back soluble sugars from ethylene treated tissue, indicating that PMR6, or its enzymatic product, in some way functions to regulate ethylene signaling. Double mutant analysis demonstrates that PMR6 functions at or below CTR1, as it is able to relieve the hook in ctr1-3. It is hypothesized that cell wall fragments alter ethylene responsive growth as evidenced by the characterization of pmr6-6, which demonstrates the ability of small sugars to serve as feedback regulators in order to control the level of ethylene response.