& Context The cause of morphological plasticity of leaves within the crowns of tall trees still debated. Whether it is driven by irradiance or hydraulic constraints is inconclusive. In a previous study, we hypothesized that water stress caused between-site and within-tree morphological variability in mature Robinia trees. & Aims To test this hypothesis, we designed an experiment to analyze the effect of long-term water stress on leaf growth of Robinia seedlings in a controlled environment. & Methods Two treatments were performed: well-watered (midday water potential, Ψ w =−0.45 MPa) and waterstressed (Ψ w =−1.0 Mpa), which resulted in significant differences in physiology, relative growth rate, and the temporal progress of leaf growth.

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Leaf morphology in the upper canopy of trees tends to be different from that lower down. The effect of long-term water stress on leaf growth and morphology was studied in seedlings of Metasequoia glyptostroboides to understand how tree height might affect leaf morphology in larger trees. Tree height increases water stress on growing leaves through increased hydraulic resistance to water flow and increased gravitational potential, hence we assume that water stress imposed by soil dehydration will have an effect equivalent to stress induced by height. Seedlings were subjected to well-watered and two constant levels of long-term water stress treatments. Drought treatment significantly reduced final needle count, area and mass per area (leaf mass area, LMA) and increased needle density. Needles from water-stressed plants had lower maximum volumetric elastic modulus (ε(max)), osmotic potential at full turgor (Ψ¹⁰⁰(π)) (and at zero turgor (Ψ⁰(π)) (than those from well-watered plants. Palisade and spongy mesophyll cell size and upper epidermal cell size decreased significantly in drought treatments. Needle relative growth rate, needle length and cell sizes were linear functions of the daily average water potential at the time of leaf growth (r² 0.88-0.999). We conclude that water stress alone does mimic the direction and magnitude of changes in leaf morphology observed in tall trees. The results are discussed in terms of various models for leaf growth rate.

Background Gastrodin (GAS), is a kind of phenolic compound extracted from the traditional Chinese herbal medicine Gastrodia elata Blume (GEB). This study was aimed at probing into the protective effect of GAS on peripheral nerve injury (PNI) and the underlying mechanism. Methods A rat model with PNI was established, followed by intraperitoneal injection of GAS (20 mg/kg/day). Sciatic nerve function index (SFI) was used to analyze the function of sciatic nerve. The amplitude and latency of compound muscle action potential (CMAP) were examined by electrophysiology. Schwann cells (SCs) were isolated from fetal rats and treated with GAS 200 μg/mL, and H2O2-induced model of oxidative stress injury was established. EdU and Transwell assays were adopted to detect the viability and migration of SCs. Dual-luciferase reporter gene assays were applied to verify the binding site between miR-497 and brain-derived neurotrophic factor (BDNF) 3’UTR. MiR-497 expression was probed by quantitative real-time polymerase chain reaction (qRT-PCR). BDNF, neurofilament-200 (NF-200) and myelin basic protein (MBP) expression levels were detected by Western blotting. Malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, glutathione content (GSH) and catalase (CAT) activity in SCs were also measured. Results GAS treatment could significantly increase the SFI and amplitude of CMAP, shorten the refractory period, and ameliorate muscle atrophy of the rats with PNI. GAS treatment could markedly restrain miR-497 expression and increase the expression levels of BDNF, NF-200 and MBP in SCs. BDNF was confirmed as the target of miR-497 and BDNF overexpression could reverse the impacts of miR-497 overexpression on the proliferation, migration, and oxidative stress response of SCs. Conclusions GAS promotes the recovery of PNI via modulating miR-497 / BDNF axis and inhibiting oxidative stress. Graphical abstract