A proposed model for AL PHD-PRC1 complexes in silencing seed developmental genes during seed germination.

Abstract

<p>ALs, <i>via</i> their highly conserved PHD domains, bind H3K4me3 of chromatin, triggering the recruitment of PRC1 components BMI1 and RING1 <i>via</i> AL-AtBMI1, AL-AtRING1, and AtBMI1-AtRING1 physical interactions. Next, two possible pathways (1 and 2) can lead to stable repressive chromatin state formation. In the first case (1), PRC2 is recruited <i>via</i> its subunit CLF interaction with AtRING1 and deposits H3K27me3, favoring further LHP1 recruitment <i>via</i> H3K27me3-LHP1 binding. In the second case (2), LHP1 is first recruited <i>via</i> its interaction with AtRING1 or AtBMI1, and then PRC2 is recruited <i>via</i> its subunit MSI1 interaction with LHP1 and deposits H3K27me3. In both cases, H3K27me3-LHP1 and PRC2 MSI1-LHP1 interactions form a positive loop in H3K27me3 enrichment. This hypothetic model can explain how seed developmental genes (<i>e.g. ABI3</i>, <i>DOG1</i>) are switched from active transcription to a stably repressed state, which is necessary for timely seed germination and proper seedling growth and development.</p

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