Figure 7.

A Model Illustrating Organ-Specific Regulation of SAUR16/50 During De-Etiolation.

In etiolated cotyledons, PIF proteins accumulate to interfere with the binding of TCP4-like transcription factors to the SAUR16/50 promoter regions, inhibiting TCP4-mediated activation of the SAUR genes in the dark. The inhibition of TCP4-SAUR16/50 transcription by PIFs contributes to the typically closed cotyledon phenotype of etiolated seedlings. During de-etiolation, PIF protein levels sharply decline, resulting in increased binding of TCP4 to the promoters of the SAURs and their elevated expression, which facilitates cotyledon opening. In hypocotyls, SAUR16/50 genes are regulated by a different mechanism involving auxin. These genes are highly expressed in the dark, and their expression declines upon the transition from dark to light, which is correlated with changes in auxin levels in the hypocotyl (Sun et al., 2016).