Figure 8.

Proposed model for the control of SOM expression and thermoinhibition of seed germination by AGL67 and EBS through epigenetic increase of histone acetylation levels. Under normal conditions, low levels of AGL67 and EBS cannot induce SOM expression because of the presence of a repressor complex at the SOM promoter, which maintains high GA and low ABA levels compatible with seed germination. However, HT treatment induces the accumulation of AGL67, which physically interacts with EBS at the SOM locus to epigenetically increase H4K5ac levels through the recruitment of histone acetyltransferases (HATs) to the SOM promoter. The subsequent increase in SOM transcription leads to altered GA/ABA metabolism that suppresses seed germination under HT. However, in agl67 or ebs mutant seeds, SOM cannot be induced due to the loss of AGL67 or EBS at the SOM promoter, which leaves the repressor free to occupy the SOM promoter and again block SOM expression, ultimately driving the higher germination rates under HT seen in som, ebs, and agl67 mutants.