SAUR17 and SAUR50 Differentially Regulate PP2C-D1 during Apical Hook Development and Cotyledon Opening in Arabidopsis

After germination in darkness, Arabidopsis seedlings undergo etiolation, and develop apical hooks, closed cotyledons, and fast elongating hypocotyls. Upon perceiving the light, seedlings de-etiolate, which includes opening of apical hooks and cotyledons. In this study, we identify Arabidopsis SAUR17 as a downstream effector of etiolation, which serves to bring about etiolated apical structures, i.e. apical hook and closed cotyledons. SAUR17 is highly expressed in apical hooks and cotyledons and is repressed by light. The apical organs also express a group of light-inducing SAURs as represented by SAUR50, which work to promote opening of the hook and cotyledons. Development of etiolated or de-etiolated apical structures requires asymmetric differential cell growth. We present evidence that the opposing action of SAUR17 and SAUR50 on apical development largely results from their antagonistic regulation of PP2C-D1, the phosphatase that suppresses cell expansion and promotes apical hook development in the dark. SAUR50 inhibits PP2C-D1, while SAUR17 has a higher affinity to PP2C-D1 without inhibiting its activity. We demonstrate that PP2C-D1 predominantly associates with SAUR17 in etiolated seedlings, which shields it from inhibitory SAURs such as SAUR50. Light signals turn off SAUR17 and up-regulate a subgroup of SAURs including SAUR50 at the inner side of the hook and cotyledon cells, causing cell expansion and consequently unfolding the hook and cotyledons.consequently unfolding the hook and cotyledons.