UVR8 interacts with WRKY36 to regulate HY5 transcription and hypocotyl elongation in Arabidopsis

Abstract

UV RESISTANCE LOCUS 8 (UVR8) is an ultraviolet-B (UVB) radiation photoreceptor that mediates light responses in plants. How plant UVR8 acts in response to UVB light is not well understood. Here, we report the identification and characterization of the Arabidopsis WRKY DNA-BINDING PROTEIN 36 (WRKY36) protein. WRKY36 interacts with UVR8 in yeast and Arabidopsis cells and it promotes hypocotyl elongation by inhibiting HY5 transcription. Inhibition of hypocotyl elongation under UVB requires the inhibition of WRKY36. WRKY36 binds to the W-box motif of the HY5 promoter to inhibit its transcription, while nuclear localized UVR8 directly interacts with WRKY36 to inhibit WRKY36-DNA binding both in vitro and in vivo, leading to the release of inhibition of HY5 transcription. These results indicate that WRKY36 is a negative regulator of HY5 and that UVB represses WRKY36 via UVR8 to promote the transcription of HY5 and photomorphogenesis. The UVR8-WRKY36 interaction in the nucleus represents a novel mechanism of early UVR8 signal transduction in Arabidopsis.

UV‐B photoreceptor UVR8 interacts with MYB73/MYB77 to regulate auxin responses and lateral root development

“…To examine whether UV‐B‐activated UVR8 affects root growth, we grew wild‐type (WT) Arabidopsis plants on 1/2 Murashige and Skoog (MS) plates under continuous white light and under white light plus UV‐B conditions and analyzed root development. UV‐B treatment not only inhibited hypocotyl elongation (Liang et al , ; Yang et al , 2018b), but also negatively regulated the growth of lateral roots (Fig A). The lateral root density of the WT was dramatically (about 3.6 times) lower under the UV‐B treatment than without (Fig B), and in the presence of UV‐B, the lateral root density of the WT was much lower than that of uvr8 (deficient in UVR8) but much higher than that of rup1 rup2 (deficient in RUP1 and RUP2 that mediate UVR8 re‐dimerization; Fig B).…”

“…An in vitro pull‐down assay was also applied to test the interaction between UVR8 and MYB73/MYB77. UVR8 and MYB73/MYB77 were expressed and purified as reported previously (Yang et al , 2018b). More MYB73/MYB77 was pulled down with UVR8 in the presence of UV‐B light than without it (Fig A and B), indicating that UVR8 interacts with MYB73/MYB77 in a UV‐B‐enhanced manner in vitro .…”

“…UVR8 also physically interacts with transcription factors BES1, BIM1, and WRKY36 in the nucleus in a UV‐B‐independent manner, while only the UV‐B‐activated monomeric UVR8 inhibits their DNA‐binding activity to regulate transcription and photomorphogenesis (Liang et al , ; Yang et al , 2018b). It was previously unknown, however, whether UVR8 interacted with some transcription factors in a UV‐B‐dependent manner.…”

“…The WD40‐repeat proteins REPRESSOR OF UV‐B PHOTOMORPHOGENESIS (RUP1) and RUP2 physically interact with UVR8 to disrupt the UVR8–COP1 interaction and mediate UVR8 re‐dimerization (Gruber et al , ). UVR8 also physically interacts with the transcription factors BES1, BIM1, and WRKY36 in the nucleus, directly regulating the transcription of their target genes and photomorphogenesis (Liang et al , ; Yang et al , 2018b). Whether or not UVR8 interacts with transcription factors in a UV‐B‐dependent manner and directly regulates transcription is unknown.…”

Plant photoreceptors and their signaling components compete for COP 1 binding via VP peptide motifs

“…It is interesting to note that the COP1 Tyr441Ala mutant still shows UV‐B‐dependent hypocotyl growth inhibition even though the COP1 Tyr441Ala protein is impaired in its interaction with UVR8. This UV‐B response is possibly due to a recently described COP1‐independent UVR8 activity involving direct interaction and inhibition of transcription factors that promote hypocotyl elongation (Liang et al , ; Yang et al , ). Moreover, we cannot exclude that the UVR8 interaction with COP1 that is independent of the UVR8 C‐terminal VP domain (Fig D, Appendix Fig S4B and Fig EV2B; see also Yin et al , ) can affect COP1 Tyr441Ala activity sufficiently to see a long‐term phenotype such as hypocotyl growth inhibition.…”