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

Abstract

Abscisic acid (ABA) transport plays a crucial role in seed germination under unfavourable conditions such as cold stress. Both heat shock protein 70 (HSP70) and voltage-dependent anion channel (VDAC) protein are involved in cold stress responses in Arabidopsis. However, their roles in seed germination with regard to ABA signaling remain unknown. Here we demonstrated that Arabidopsis HSP70-16 and VDAC3 jointly suppress seed germination under cold stress conditions. At 4°C, 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 study reveals that HSP70-16 interacts with VDAC3 and facilitates the opening of the VDAC3 ion channel, which influences ABA efflux from endosperm to embryo, thus negatively regulates seed germination under cold stress.