PIF7 controls leaf cell proliferation through an AN3 substitution-39 repression mechanism

Ejaz Hussain, Andres Romanowski, Karen J. Halliday

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Plants are agile, plastic organisms able to adapt to everchanging circumstances. Responding to far-red (FR) wavelengths from nearby vegetation, shade-intolerant species elicit the adaptive shade-avoidance syndrome (SAS), characterized by elongated petioles, leaf hyponasty, and smaller leaves. We utilized end-of-day FR (EODFR) treatments to interrogate molecular processes that underlie the SAS leaf response. Genetic analysis established that PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) is required for EODFR-mediated constraint of leaf blade cell division, while EODFR messenger RNA sequencing data identified ANGUSTIFOLIA3 ( AN3) as a potential PIF7 target. We show that PIF7 can suppress AN3 transcription by directly interacting with and sequestering AN3. We also establish that PIF7 and AN3 impose antagonistic control of gene expression via common cis-acting promoter motifs in several cell-cycle regulator genes. EODFR triggers the molecular substitution of AN3 to PIF7 at G-box/PBE-box promoter regions and a switch from promotion to repression of gene expression.

Original languageEnglish
Article numbere2115682119
Number of pages11
JournalProceedings of the National Academy of Sciences (PNAS)
Volume119
Issue number5
Early online date27 Jan 2022
DOIs
Publication statusPublished - 1 Feb 2022

Keywords / Materials (for Non-textual outputs)

  • AN3
  • EODFR
  • PIF7
  • leaf development
  • cell proliferation

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