The Arabidopsis EIN3 Binding F-Box Proteins EBF1 and EBF2 Have Distinct but Overlapping Roles in Ethylene Signaling

Abstract

Ethylene signaling in Arabidopsis thaliana converges on the ETHYLENE-INSENSITIVE3 (EIN3)/EIN3-Like (EIL) transcription factors to induce various responses. EIN3 BINDING F-BOX1 (EBF1) and EBF2 were recently shown to function in ethylene perception by regulating EIN3/EIL turnover. In the absence of ethylene, EIN3 and possibly other EIL proteins are targeted for ubiquitination and subsequent degradation by Cullin 1-based E3 complexes containing EBF1 and 2. Ethylene appears to block this ubiquitination, allowing EIN3/EIL levels to rise and mediate ethylene signaling. Through analysis of mutant combinations affecting accumulation of EBF1, EBF2, EIN3, and EIL1, we show that EIN3 and EIL1 are the main targets of EBF1/2. Kinetic analyses of hypocotyl growth inhibition in response to ethylene and growth recovery after removal of the hormone revealed that EBF1 and 2 have temporally distinct but overlapping roles in modulating ethylene perception. Whereas EBF1 plays the main role in air and during the initial phase of signaling, EBF2 plays a more prominent role during the latter stages of the response and the resumption of growth following ethylene removal. Through their coordinated control of EIN3/EIL1 levels, EBF1 and EBF2 fine-tune ethylene responses by repressing signaling in the absence of the hormone, dampening signaling at high hormone concentrations, and promoting a more rapid recovery after ethylene levels dissipate.

Direct transcriptional control of the Arabidopsis immune receptor FLS2 by the ethylene-dependent transcription factors EIN3 and EIL1

“…4D). The effect of single mutations in EIN3 and EIL transcription factors is often hindered by their homology and consequent functional redundancy (17,26,27). Indeed, simultaneous mutations in EIN3 and EIL1 accentuated the effect on FLS2 expression, with the double mutant ein3-1 eil1-1 accumulating as little FLS2 transcript as the ein2-5 mutant (Fig.…”

Interaction between MYC2 and ETHYLENE INSENSITIVE3 Modulates Antagonism between Jasmonate and Ethylene Signaling inArabidopsis

“…The Arabidopsis thaliana mutants coi1-1 (Xie et al, 1998), coi1-2 (Xu et al, 2002, JAZ1D3A (Thines et al, 2007), myc2-2 (Boter et al, 2004, jin1-2 (Lorenzo et al, 2004), myc3 (GK445B11) (Fernández-Calvo et al, 2011), myc4 (GK491E10) (Fernández-Calvo et al, 2011), jin1-2 myc3 myc4 (Fernández-Calvo et al, 2011), eto1-1 (Guzmán andEcker, 1990), ctr1-1 (Kieber et al, 1993), ein2-1 (Alonso et al, 1999), hls1-1 (Lehman et al, 1996), ein3-1 (Chao et al, 1997), eil1-3/Salk_049679 (Binder et al, 2007), myb21 myb24 myb57 , and gl3 egl3 tt8 were previously described. The higher order mutants myc2-2 myc3, myc2-2 myc4, myc2-2 myc3 myc4, ein3-1 eil1-3, coi1-2 ein3-1 eil1-3, coi1-2 hls1-1, myc2-2 ein3 eil1-3, and jin1-2 myc3 myc4 ein3-1 eil1-3 were generated by genetic crosses using standard techniques.…”

ETHYLENE-INSENSITIVE3 Is a Senescence-Associated Gene That Accelerates Age-Dependent Leaf Senescence by Directly Repressing miR164 Transcription in Arabidopsis

“…Because EIN3 and its close homolog EIL1 functionally overlap (Chao et al, 1997;Tieman et al, 2001;Binder et al, 2007;An et al, 2010), we studied ein3 eil1 double mutants instead of ein3 single mutants, to preclude the functional redundancy and the possibly compromised phenotype of the single mutants (see below). Compared with the wild type, ein3 eil1 plants exhibited a delayed-senescence phenotype ( Figure 2A).…”

“…In addition to EIN3, the Arabidopsis genome encodes five EIN3-Like (EIL) transcription factors (Chao et al, 1997), wherein EIN3 and EIL1, its closest homolog, seem to mediate the vast majority of ethyleneregulated processes (Alonso et al, 2003;Binder et al, 2004). Genetic and biochemical studies revealed that EIN3 and EIL1 functions overlap, and both are subject to proteasomal degradation mediated by the F-box proteins EIN3-BINDING F BOX PROTEIN1 (EBF1) and EBF2 in the absence of ethylene signal (Guo and Ecker, 2003;Potuschak et al, 2003;Gagne et al, 2004;Binder et al, 2007;An et al, 2010).…”