Sometimes new results raise new questions: the question marks between mitogen-activated protein kinase and ethylene signaling

Abstract

In Arabidopsis thaliana, mitogen activated protein kinase (MAPK) signaling cascades that contain MPK3, MPK4 and MPK6 have been implicated in various aspects of developmental processes and stress responses. We identified an ethylene response factor (ERF104), which controls innate immunity, to be a specific substrate of MPK6 and showed that ethylene signaling regulates the release of the ERF104 substrate from its kinase. Implications and questions that arise from our findings are addressed. To promote discussions, previously unpublished data, that are rather confounding, are presented and possible explanation provided on how these may fit into our current model.

Figure 1

Models showing positions of the flg22-induced ET biosynthesis with respect to MAPK components. In model 1, ET is rapidly produced after recognition of flg22 by the FLS2 receptor and leads to MAPK activation. Activated MPK6 may feedback positively on the ET biosynthesis in the cytoplasm and at the same time, some nuclear-translocated MPK6 could act on its substrates such as ERF104. Thus, the loss of MPK6/ERF104 interaction reflects the enzyme-substrate reaction dynamics. In the alternative model 2, activation of the MAPK cascade is independent of the ET signal but the activated MPK6 generates an ET signal through stabilization of the ACC synthases, ACS2/ACS6. Nuclear-translocated MPK6 interacts with ERF104, phosphorylates it but requires the ET signal generated by cytoplasmic MPK6 to release ERF104 (indicated by dashed arrow). Model 2 is compatible with findings in mpk6 mutants, where reduced flg22-induced ET biosynthesis occurs, and hence no disruption of the nuclear MPK6/ERF104 complex is seen.

Figure 2

FRET analysis of ERF104/MPK6 interaction in an mpk6 mutant background. Unlike in protoplasts derived from wild-type plants, flg22 does not cause disruption of ERF104/MPK6 complex. ACC, the ET precursor, can cause complex disruption, suggesting that ET accumulation may be the missing factor in these mpk6 cells.