MYBD employed by HY5 increases anthocyanin accumulation via repression of MYBL2 in Arabidopsis

Abstract

SUMMARYPhotomorphogenesis is an essential program in plant development. This process is effected by the balanced cooperation of many factors under light and dark conditions. In a previous study, we showed that MYB hypocotyl elongation-related (MYBH) is involved in cell elongation. To expand our understanding of MYBH function, we performed a yeast two-hybrid assay and identified an MYB-like Domain transcription factor (MYBD). In this study, we investigated the function of MYBD, which is an MYBH homolog involved in anthocyanin accumulation. MYBD expression increased in response to light or cytokinin, and MYBD enhanced anthocyanin biosynthesis via repression of MYBL2, which encodes a transcription factor that has a negative effect on this process. In addition, MYBD binding in vivo to the MYBL2 promoter and the lower level of histone H3K9 acetylation at the upstream region of MYBL2 in MYBD over-expressing plants in comparison with wild-type plants imply that MYBD represses MYBL2 expression via an epigenetic mechanism. HY5 directly binds to the MYBD promoter, which indicates that MYBD acts on HY5-downstream in light-or cytokinintriggered signaling pathways, leading to anthocyanin accumulation. Our results suggest that, although MYBD and MYBH are homologs, they act in opposite ways during plant photomorphogenesis, and these functions should be examined in further studies.

MYB-related transcription factors function as regulators of the circadian clock and anthocyanin biosynthesis in Arabidopsis

“…29 Our recent study found that AtMYBD may also regulate MYBL2 expression in a diurnal manner leading to anthocyanin accumulation in the plant. 17 Taken together, our results suggest that AtMYBD may also work as a regulator of anthocyanin accumulation in a circadian-dependent manner. This speculation still requires further studies to validate it.…”

“…[14][15][16] Currently, we have found that AtMYBD expression is also controlled by diurnal regulation, see ref. 17 , and this implies that the AtMYBD transcription factor may function to control downstream processes in a circadian clock-dependent manner.…”

“…For example, MYB11, MYB12, MYB111, MYB75/ PAP1, and AtMYBD work as positive regulators whereas MYB-LIKE 2 (MYBL2) functions as a negative regulator. 17,19,[27][28][29][30] Among them, MYB75/PAP1 is a master regulator of the anthocyanin biosynthesis pathway; 19,31 however, direct evidence reflecting whether or not PAP1 can act on the circadian regulation of this biosynthesis pathway is still lacking. 32 Currently, a study has revealed that 2 circadian components NIGHT LIGHT-INDUCIBLE AND CLOCK-REGULATED (LNK) and RVE8 collaborate to control the anthocyanin metabolic pathway.…”

Genome-wide analysis of cis-regulatory element structure and discovery of motif-driven gene co-expression networks in grapevine

“…In addition, genes involved in the glycosylation of flavonols—essential for enhancing their solubility in water and accumulation in plant cells 68 —namely VviGT5 (VIT_11s0052g01630) and VviGT6 (VIT_11s0052g01600), were connected with VviHYH within one and two steps, respectively. An Arabidopsis MYB-like domain TF homolog ( VviMYBD , VIT_01s0026g01050), involved in the regulation of anthocyanin biosynthesis, 69 was also co-regulated with VviHYH ( k  =   2). These observations reaffirm the involvement of VviHYH submodule genes in light-regulated transcriptional and secondary metabolism networks in a stress-related context.…”

Identification of Candidate Anthocyanin-Related Genes by Transcriptomic Analysis of ‘Furongli’ Plum (Prunus salicina Lindl.) during Fruit Ripening Using RNA-Seq

“…Its Arabidopsis homolog (AtMYB113) is an activator of the anthocyanin pathway. Recently, AtMYBD was shown to enhance anthocyanin biosynthesis by repressing the negative regulator MYBL2 (Nguyen et al, 2015). The expression of an AtMYBD homolog (c28480.graph_c0) was upregulated in late ripening stages, but it does not show significant correlation with any structural genes.…”