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May 9, 2026Journal of Integrative Plant Biology1 citations

A group of TCP transcription factors is a missing link in strigolactone signaling

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YHYi HuangLBLumei BiYHYongshuang Huang

Key Points

  • This study aims to investigate the role of TCP transcription factors in strigolactone signaling and their impact on plant development.
  • Constructed a chromatin co-localization map of SMXL6 with 108 transcription factors.
  • Analyzed TCP4's interaction with SMXL6 at SL-induced target gene promoters.
  • Evaluated the effects of tcp3/4/10 on SL-deficient mutants.
  • TCP4 co-localizes with SMXL6 at the promoter regions of 18 SL-induced target genes.
  • Loss of CIN-TCPs function decreases SL-induced gene responsiveness, indicating TCP roles in hormone signaling.
  • Introducing tcp3/4/10 into SL-deficient mutants restored BRC1 expression, but branching control was only partially rescued, suggesting the need for other factors.

Abstract

ABSTRACT Strigolactones (SLs) are plant‐specialized butenolide signaling molecules, recognized as endogenous plant hormones, that control plant development and environmental adaptation. In Arabidopsis ( Arabidopsis thaliana ), the repressor D53‐like SMXLs regulate the expression of a vast number of genes in an EAR‐motif‐dependent manner to mediate SL signaling. However, it remains unclear how the SMXLs are recruited to specific genes and implement unique functions in vivo . Based on chromatin co‐distribution analysis, we constructed a chromatin co‐localization map of SMXL6 with 108 transcription factors. Among the candidate transcription factors, the Class II TEOSINTE BRANCHED1/CYCLOIDEA/PCF (TCP) family member TCP4 shows the highest frequency of chromatin co‐localization with SMXL6. SMXL6 and TCP4 co‑localize at the promoter regions of 18 SL‐induced SMXL6 target genes (SISGs), including BRC1 . We confirmed that TCP4 interacts with SMXL6 and can bind directly to these co‑localized sites. The loss of CIN‐TCPs function reduces the hormone responsiveness of the SL‐induced genes. Introducing the tcp3/4/10 into SL‑deficient mutants restored the BRC1 expression to a level exceeding that of the wild type. However, the branching phenotype of the SL‑deficient mutant was only partially rescued, suggesting a limited role for BRC1 in SL‑mediated branching control and implicating the involvement of additional factors. An unexpected finding was that tcp3/4/10 rescued the dwarf phenotype of the SL‑deficient mutants, providing an opportunity to elucidate the mechanisms underlying SL‑regulated plant height. These findings demonstrate that TCP4 mediates SMXL6 chromatin recruitment during SL signaling, and provide a new understanding of how SMXL6 participates in SL signaling‐mediated gene expression and plant development.

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Cite This Study

Huang et al. (2026) studied this question.

synapsesocial.com/papers/69fed0e2b9154b0b8287801ahttps://doi.org/10.1111/jipb.70281
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