Key message <p>Genome-wide analysis coupled with spatiotemporal profiling identified <i>CmMYC25</i> as a key regulator. It functions as a transcriptional co-activator to synergistically enhance CmMYB6-mediated anthocyanin biosynthesis in chrysanthemum petals.</p> Abstract <p>Myelocytomatosis (MYC) transcription factors (TFs), belonging to the basic helix-loop-helix (bHLH) superfamily, play a crucial role in regulating various physiological processes in plants. However, research on the <i>MYC</i> gene family in <i>Chrysanthemum morifolium</i>, one of the primary cut flowers, remains scarce. Here, we identified 28 CmMYC genes via genome-wide analysis and classified them into three subfamilies based on phylogenetic relationships. Collinearity analysis suggested expansion driven by both ancient whole-genome duplication (WGD) events and recent segmental duplications. Promoter analysis uncovered a variety of regulatory elements, with hormone-responsive motifs being the most predominant. Phylogenetic clustering indicated that Group B members are orthologous to anthocyanin regulators. Among them, CmMYC25 was prioritized for further analysis, as its expression pattern was perfectly synchronized with anthocyanin accumulation during flower development. CmMYC25 was localized to the nucleus but lacked transcriptional activation activity. Notably, yeast one-hybrid assays indicated that CmMYC25 does not directly bind to the promoters of anthocyanin biosynthetic genes. Instead, it physically interacts with CmMYB6, a central activator of anthocyanin biosynthesis. Dual-luciferase assays confirmed that CmMYC25 functions as a co-activator, synergistically enhancing the transcriptional activity of CmMYB6 on downstream target genes. Functional characterization verified that CmMYC25 acts as a positive regulator of floral pigmentation, as its overexpression significantly increased anthocyanin accumulation, while suppression reduced pigmentation. These findings provide insights into the evolution of CmMYC genes and elucidate the co-activator mechanism of CmMYC25 in regulating flower pigmentation.</p>

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Genome-wide identification of MYC transcription factors in Chrysanthemum morifolium and CmMYC25 promotes petal anthocyanin accumulation

  • Wenhao Xia,
  • Yuxi Wang,
  • Ge Zhao,
  • Jialin Peng,
  • Xiuge Li,
  • Yukun Li,
  • Yuhe Tian,
  • Aiping Song,
  • Sumei Chen,
  • Fadi Chen,
  • Li-Jie Zhou

摘要

Key message

Genome-wide analysis coupled with spatiotemporal profiling identified CmMYC25 as a key regulator. It functions as a transcriptional co-activator to synergistically enhance CmMYB6-mediated anthocyanin biosynthesis in chrysanthemum petals.

Abstract

Myelocytomatosis (MYC) transcription factors (TFs), belonging to the basic helix-loop-helix (bHLH) superfamily, play a crucial role in regulating various physiological processes in plants. However, research on the MYC gene family in Chrysanthemum morifolium, one of the primary cut flowers, remains scarce. Here, we identified 28 CmMYC genes via genome-wide analysis and classified them into three subfamilies based on phylogenetic relationships. Collinearity analysis suggested expansion driven by both ancient whole-genome duplication (WGD) events and recent segmental duplications. Promoter analysis uncovered a variety of regulatory elements, with hormone-responsive motifs being the most predominant. Phylogenetic clustering indicated that Group B members are orthologous to anthocyanin regulators. Among them, CmMYC25 was prioritized for further analysis, as its expression pattern was perfectly synchronized with anthocyanin accumulation during flower development. CmMYC25 was localized to the nucleus but lacked transcriptional activation activity. Notably, yeast one-hybrid assays indicated that CmMYC25 does not directly bind to the promoters of anthocyanin biosynthetic genes. Instead, it physically interacts with CmMYB6, a central activator of anthocyanin biosynthesis. Dual-luciferase assays confirmed that CmMYC25 functions as a co-activator, synergistically enhancing the transcriptional activity of CmMYB6 on downstream target genes. Functional characterization verified that CmMYC25 acts as a positive regulator of floral pigmentation, as its overexpression significantly increased anthocyanin accumulation, while suppression reduced pigmentation. These findings provide insights into the evolution of CmMYC genes and elucidate the co-activator mechanism of CmMYC25 in regulating flower pigmentation.