ABSCISIC ACID-INSENSITIVE 5 (ABI5) Orchestrates Seasonal Growth Cessation and Wood Formation Inhibition in Populus tomentosa

TL;DR

This study shows how the PtoABI5 gene in poplar trees helps control seasonal growth and wood formation by linking two plant hormones, ABA and GA.

Contribution

The study identifies PtoABI5 as a key regulator connecting ABA and GA signaling in seasonal growth cessation and wood formation in poplar.

Findings

PtoABI5 overexpression mimics and intensifies short-day responses, causing early growth cessation and reduced wood formation.

PtoABI5 suppresses GA biosynthesis genes and enhances GA catabolic genes, linking ABA and GA pathways.

Exogenous GA application partially reverses the growth and wood formation defects caused by PtoABI5 overexpression.

Abstract

Perennial trees in temperate regions precisely coordinate the timing of seasonal growth cessation and dormancy with environmental cues, primarily photoperiod. While the roles of abscisic acid (ABA) in dormancy regulation are well-established, its function in growth cessation remains less defined. ABSCISIC ACID-INSENSITIVE 5 (ABI5) is a basic leucine zipper transcription factor that plays a central role in ABA-mediated development and abiotic stress responses, yet its roles in photoperiodic regulation of growth cessation and its coordination with radial stem growth remain unknown. Here, we demonstrate that in poplar (Populus tomentosa) trees, exogenous ABA application exacerbated short-day (SD)-induced growth inhibition, accelerated bud set, and strongly suppressed secondary xylem formation. We identified a Populus ABI5 homolog, PtoABI5, whose expression is induced by both ABA and SDs. Overexpression of PtoABI5 phenocopied and enhanced SD responses, leading to premature growth cessation and a pronounced inhibition of cambial division and wood formation under SDs. Conversely, PtoABI5 suppressed the expression of the GA biosynthesis gene, while it enhanced the expression of GA catabolic genes. Exogenous GA application partially rescued both the apical growth defects and the impaired secondary xylem development in PtoABI5-overexpressing plants. Our findings establish PtoABI5 as a central integrator, linking ABA and GA signaling pathways to coordinately arrest shoot apical growth and seasonal wood formation, thereby fine-tuning the seasonal growth cycle in perennial trees.

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