Hormones play a critical role throughout the entire life cycle of plants. The gas ethylene is, together with auxin, one of the earliest characterized plant hormones. Ethylene distinguishes itself among the other plants hormones by its simple hydrocarbon structure (C2H4) and its gaseous nature. This simple molecule, however, plays a major role in plant growth and development by influencing a wide range of complex physiological processes throughout the entire plant life cycle, from seed germination to flowering, fruit ripening, and senescence. A basic challenge in biology is, therefore, to understand the molecular mechanisms that underlie ethylene action. Ethylene signaling begins with ethylene binding to and inactivating a family of ethylene receptors. In the absence of ethylene, these receptors activate CTR1 a MAPKKK (mitogen activating protein kinase kinase kinase) that negatively regulates the pathway. After the inactivation of CTR1, EIN2 promotes ethylene responses via the downstream transcription factor EIN3 and most likely also via its close homolog EIL1. EIN3 activates primary targets of the ethylene response cascade such as ERF1. Recent work by Ortega-Martinez et al. (2008) suggest a role of ethylene signaling in the regulation of stem cell fate. Furthermore the phenotype of ebf1ebf2 hypomorphic double mutants, that have over-accumulation of EIN3 protein, shows several strong developmental defects such as pronounced dwarfism, abnormally small flowers with protruding gynoecium, rosettes with small sized leaves and male sterility. In addition ebf1ebf2 double null mutants have been described that are seedling lethal and develop disorganized tumor-like shoot tissue, a feature previously unknown for ethylene mutants. In this project, we propose to investigate the role of EIN3 during ethylene response using molecular and genetic approaches.
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