The COP9 Signalosome regulates seed germination by facilitating protein degradation of RGL2 and ABI5

<div><p>The control of seed germination and seed dormancy are critical for the successful propagation of plant species, and are important agricultural traits. Seed germination is tightly controlled by the balance of gibberellin (GA) and abscisic acid (ABA), and is influenced by environmental factors. The COP9 Signalosome (CSN) is a conserved multi-subunit protein complex that is best known as a regulator of the Cullin-RING family of ubiquitin E3 ligases (CRLs). Multiple viable mutants of the CSN showed poor germination, except for <i>csn5b-1</i>. Detailed analyses showed that <i>csn1-10</i> has a stronger seed dormancy, while <i>csn5a-1</i> mutants exhibit retarded seed germination in addition to hyperdormancy. Both <i>csn5a-1</i> and <i>csn1-10</i> plants show defects in the timely removal of the germination inhibitors: RGL2, a repressor of GA signaling, and ABI5, an effector of ABA responses. We provide genetic evidence to demonstrate that the germination phenotype of <i>csn1-10</i> is caused by over-accumulation of RGL2, a substrate of the SCF (CRL1) ubiquitin E3 ligase, while the <i>csn5a-1</i> phenotype is caused by over-accumulation of RGL2 as well as ABI5. The genetic data are consistent with the hypothesis that CSN5A regulates ABI5 by a mechanism that may not involve CSN1. Transcriptome analyses suggest that <i>CSN1</i> has a more prominent role than <i>CSN5A</i> during seed maturation, but <i>CSN5A</i> plays a more important role than <i>CSN1</i> during seed germination, further supporting the functional distinction of these two <i>CSN</i> genes. Our study delineates the molecular targets of the CSN complex in seed germination, and reveals that CSN5 has additional functions in regulating ABI5, thus the ABA signaling pathway.</p>