Liana attachment to supports leads to profound changes in xylem anatomy and transcriptional profile of cambium and differentiating xylem.

Wood serves crucial functions in plants, yet our understanding of the mechanisms governing the composition, arrangement, and dimensions of its cells remains limited. The abrupt transition from nonlianescent to lianescent xylem in lianas represents an excellent model to address the underlying mechanisms, although consistent triggering factors for this process remain uncertain. In this study we examined how physical support attachment impacts the development of lianescent xylem in Bignonia magnifica (Bignoniaceae), employing a comprehensive approach integrating detailed anatomical analysis with gene expression profiling of cambium and differentiating xylem. Our findings demonstrate that attachment to physical supports triggers the formation of lianescent xylem, leading to increased vessel size, broader vessel distribution, reduced fibre content, and higher potential specific water conductivity than nonlianescent xylem. These shifts in wood anatomy coincide with the downregulation of genes associated with cell division and cell wall biosynthesis, and the upregulation of transcription factors, defense/cell death, and hormone‐responsive genes in the lianescent xylem. Our findings provide insights into the regulation of xylem differentiation, driven by response to environmental stimuli. Additionally, they shed light on the mechanisms underlying the adaptation of lianas to climbing. Summary Statement: The drastic change in wood anatomy in woody vines offers an excellent model for studying wood differentiation and the adaptation of vines to climbing. In Bignonia magnifica (Bignoniaceae), attachment to supports triggers increased vessel size, broader vessel distribution, reduced fibre content, and higher water conductivity. These changes coincide with the downregulation of genes for cell division and cell wall biosynthesis, and the upregulation of transcription factors, defense/cell death, and hormone‐responsive genes. [ABSTRACT FROM AUTHOR]