Actin filaments mediated root growth inhibition by changing their distribution under UV-B and hydrogen peroxide exposure in Arabidopsis

Meiting Du,Huize Chen,Rong Han,Yanhong Wang

doi:10.1186/s40659-020-00321-3

Abstract

BackgroundUV-B signaling in plants is mediated by UVR8, which interacts with transcriptional factors to induce root morphogenesis. However, research on the downstream molecules of UVR8 signaling in roots is still scarce. As a wide range of functional cytoskeletons, how actin filaments respond to UV-B-induced root morphogenesis has not been reported. The aim of this study was to investigate the effect of actin filaments on root morphogenesis under UV-B and hydrogen peroxide exposure in Arabidopsis.ResultsA Lifeact-Venus fusion protein was used to stain actin filaments in Arabidopsis. The results showed that UV-B inhibited hypocotyl and root elongation and caused an increase in H2O2 content only in the root but not in the hypocotyl. Additionally, the actin filaments in hypocotyls diffused under UV-B exposure but were gathered in a bundle under the control conditions in either Lifeact-Venus or uvr8 plants. Exogenous H2O2 inhibited root elongation in a dose-dependent manner. The actin filaments changed their distribution from filamentous to punctate in the root tips and mature regions at a lower concentration of H2O2 but aggregated into thick bundles with an abnormal orientation at H2O2 concentrations up to 2 mM. In the root elongation zone, the actin filament arrangement changed from lateral to longitudinal after exposure to H2O2. Actin filaments in the root tip and elongation zone were depolymerized into puncta under UV-B exposure, which showed the same tendency as the low-concentration treatments. The actin filaments were hardly filamentous in the maturation zone. The dynamics of actin filaments in the uvr8 group under UV-B exposure were close to those of the control group.ConclusionsThe results indicate that UV-B inhibited Arabidopsis hypocotyl elongation by reorganizing actin filaments from bundles to a loose arrangement, which was not related to H2O2. UV-B disrupted the dynamics of actin filaments by changing the H2O2 level in Arabidopsis roots. All these results provide an experimental basis for investigating the interaction of UV-B signaling with the cytoskeleton.

Highlights

Ultraviolet B (UV-B) signaling in plants is mediated by UV resistance locus 8 (UVR8), which interacts with transcriptional factors to induce root morphogenesis
The dynamics of actin filaments in the control root under UV-B exposure showed the same tendency observed after excess H2O2 treatments, which was very different from the dynamics observed in the uvr8 root. These results indicated that the inhibition of hypocotyl elongation under UV-B exposure changed the arrangement of actin filaments, which was not related to H 2O2 production
Distribution of actin filaments in different transgenic lines Since we focused on the response of actin filaments to environmental factors in Arabidopsis thaliana roots, we tried to select a transgenic line that could be used to better observe actin filaments in roots from the fABD2-GFP and Lifeact-Venus transgenic lines

Summary

Introduction

UV-B signaling in plants is mediated by UVR8, which interacts with transcriptional factors to induce root morphogenesis. Research on the downstream molecules of UVR8 signaling in roots is still scarce. As a wide range of functional cytoskeletons, how actin filaments respond to UV-B-induced root morphogenesis has not been reported. The UVR8 protein directly and rapidly binds to COP1 (Constitutively Photomorphogenic 1) in the nucleus, and this depends on UV-B. After UVR8 binds to COP1, the expression of the transcription factor HY5/HYH (Elongated Hypocotyl 5/HY5 Related Homolog) is initiated. UVR8 can interact with multiple transcription factors, such as WRKY36 (WRKY DNA-binding protein 36), BIM1 (BES1-interacting MYC-like 1), and BES1 (BRI1-EMS-suppressor 1), to directly regulate gene expression [5]. Researchers found that BR signaling inhibits UV-B stress responses in Arabidopsis thaliana and various crops by controlling flavanol biosynthesis [6]

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