Fig. 8

Model depicting the putative role of AL6 in the response to JA. Upper panel: Under all conditions, hypocotyls of al6 seedlings were longer than those of the wild type. Exogenous JA application represses hypocotyl elongation in etiolated seedlings, a response which is dampened in the absences of sufficient Pi. Based on previously published information [27, 31, 32], a possible scenario, which awaits further experimental experimentation, can be envisaged in which AL6, and possibly other members of the AL family, recognises H3K4me3 and recruits core components of PRC1. The PRC1 reader component LHP1 interacts with PRC1 core components, and supports repressive chromatin state formation via a shift from H3K4me3 to H3K27me3, mediated by PRC2. In the absence of JA, LHP1 interacts with JAZ proteins to repress the transcription of JA-responsive genes, acting antagonistically or synergistically with LHP1-Interacting Factor 2 (LIF2), which is recruited to the nucleus by JA. Reduced abundance of AL6 compromises this shift and, possibly, leads to reduced deposition of H2A.Z caused by altered abundance of NRP1 and CHR11. The altered chromatin state leads to a partial loss of PcG silencing and modulates expression of JA-responsive genes. Black and red arrows denote up- and downregulation, respectively. Based on data reported by Molitor et al. [31,32], Li et al. [27], and results obtained in the present study