Channel deformations during elastocapillary spreading of gaseous embolisms in biomimetic leaves

TL;DR

The paper tackles embolism propagation in leaves under tension by mapping elastocapillary interactions between deformable channel ceilings and capillary forces in PDMS biomimetic leaves. It introduces a novel interferometric deformation method to infer internal pressure during pervaporation-driven embolism in 1D and 2D channel networks, grounded in Laplace-pressure thresholds. In 1D, measured pressure jumps align with theoretical predictions ($ΔP_c^{theo} ≈ $9.08×10^3 Pa) and correlate with a deformation of about $3 μm$, while 2D networks show more variable, cluster-like dynamics and lower per-constriction pressures (~6–8 kPa) than the simple theory predicts. The work demonstrates a quantitative, pressure-resolved framework for elastocapillary embolism dynamics, providing a versatile platform to explore leaf hydraulics and guiding future experiments with tunable constrictions and connectivity.

Abstract

The nucleation and/or spreading of bubbles in water under tension (due to water evaporation) can be problematic for most plants along the ascending sap network from root to leaves, named xylem. Due to global warming, trees facing drought conditions are particularly threatened by the formation of such air embolisms, which spreads intermittently and hinder the flow of sap and could ultimately result in their demise. PDMS-based biomimetic leaves simulating evapotranspiration have demonstrated that, in a linear configuration, the existence of a slender constriction in the channel allows for the creation of intermittent embolism propagation (as an interaction between the elasticity of the biomimetic leaf (mainly the deformable ceiling of the microchannels) and the capillary forces at the air/water interfaces) \cite{Keiser2022}-\cite{keiser2024}. Here we use analog PDMS-based biomimetic leaves in 1d and 2d. To better explore the embolism spreading mechanism, we add to the setup an additional technique, allowing to measure directly the microchannel's ceiling deformation versus time, which corresponds to the pressure variations. We present here such a method that allows to have quantitative insights in the dynamics of embolism spreading. The coupling between channel deformations and the Laplace pressure threshold explains the observed elastocapillary dynamics.

Figures (5)

• Figure 1: A) Image of a leaf of Walnut tree (Tahnks to Virgile Thiévenaz). B) Scheme of xylem vessel elements connected by bordered pits with embolism spreading. C) Top view of biomimetic systems with identical channels connected by narrower constrictions at various times. D) Side views (taken at black lines locations) of the deformation of the microchannels ceilings as the embolism passes through it.
• Figure 2: A) Setup with camera and spectrometer to record spectra for thickness measurements. B) Spectrum showing oscillations due to the air thicness between glass slide and ceiling of microchannel. C) Fourier trasnform of the spectrum giving a peak at the thickness measured.
• Figure 3: A) Setup for the calibration of pressure / deformation curves. B) Calibration curve on 2D systems similar to the ones used in experiments, for which different channel widths have been tested. C) Calibration curve obtained a posteriori on a channel after an experiment was done, in a 2d system and in D) for a 1d system.
• Figure 4: A) Ratio of detected white pixels in a 1D system vs. time. B) Deformation as function of time for this 1d system. C) Theoretical curves predicted in keiser2024 for the section area of channel. D) Jumps amplitude vs. time for the deformation in the measurement channel vs. time.
• Figure 5: A) Scheme of 2D device with various channel sizes. B) evolution with time of the ceiling deformation of the channel pointed in C). C) Embolism spreading with time. White domain represent the spreading air embolism. The yellow dot points the channel element where the deformation is measured over time. It correspond to the largest channels element, at the end of the main vein, the most far away from petiole (start of the embolism).