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bioRxiv · 10.1101/2021.05.31.446395

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

Hussain, E.·Romanowski, A.·Halliday, K.
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Abstract

Plants are agile, plastic organisms, able to adapt to ever-changing circumstances. Responding to far-red (FR) wavelengths from nearby vegetation, shade-intolerant species elicit the adaptive Shade Avoidance Syndrome (SAS), characterised by elongated petioles, leaf hyponasty and smaller leaves. We utilised end-of-day FR (EODFR) treatments to interrogate molecular processes that underlie the SAS leaf response. Genetic analysis establishes PHYTOCHROME INTERACTING FACTOR 7 (PIF7) is required for EODFR-mediated constraint of leaf blade cell division, while EODFR mRNAseq data identified ANGUSTIFOLIA3 (AN3) as a potential PIF7 target. We show PIF7 can suppress AN3 transcription through a sequestering mechanism that prevents AN3 activation of its own expression. We also establish 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.

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Hussain, E., Romanowski, A., Halliday, K.. 2021-05-31. PIF7 controls leaf cell proliferation through an AN3 substitution-repression mechanism. https://doi.org/10.1101/2021.05.31.446395

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