HSP70-16 and VDAC3 jointly inhibit seed germination under cold stress in 
Arabidopsis

Ashraf, Muhammad; Mao, Qionglei; Hong, Jun; Shi, Lei; Ran, Xiaoruo; Liaquat, Fiza; Uzair, Muhammad; Liang, Wanqi; Fernie, A. R.; Shi, Jianxin

doi:10.1111/pce.14138

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HSP70-16 and VDAC3 jointly inhibit seed germination under cold stress in Arabidopsis

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Fernie, A. R.
Central Metabolism, Department Willmitzer, Max Planck Institute of Molecular Plant Physiology, Max Planck Society;

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Citation

Ashraf, M., Mao, Q., Hong, J., Shi, L., Ran, X., Liaquat, F., et al. (2021). HSP70-16 and VDAC3 jointly inhibit seed germination under cold stress in Arabidopsis. Plant, Cell and Environment, 44(11), 3616-3627. doi:10.1111/pce.14138.

Cite as: https://hdl.handle.net/21.11116/0000-0008-CC85-C

Abstract

Abstract Abscisic acid (ABA) transport plays a crucial role in seed germination under unfavorable conditions such as cold stress. Heat shock protein 70 (HSP70) and voltage-dependent anion channel (VDAC) protein are both involved in cold stress responses in Arabidopsis. However, their roles in seed germination with regard to ABA signaling remains unknown. Here we demonstrated that Arabidopsis HSP70-16 and VDAC3 jointly suppress seed germination under cold stress conditions. At 4oC, both HSP70-16 and VDAC3 facilitated the efflux of ABA from the endosperm to the embryo and thus inhibited seed germination. HSP70-16 interacted with VDAC3 on the plasma membrane and in the nucleus, and the interplay between HSP70-16 and VDAC3 activated the opening of the VDAC3 ion channel. Our work established a novel function of HSP70-16 in seed germination under cold stress and a possible association of VDAC3 activity with ABA transportation from endosperm to embryo under cold stress conditions. This article is protected by copyright. All rights reserved.