The translocase of the inner mitochondrial membrane 22-2 (AtTIM22-2) is required for mitochondrial membrane functions during Arabidopsis seed development.

The carrier translocase (also known as translocase of the inner membrane 22; TIM22 complex) is an important component of the mitochondrial protein import apparatus. However, the biological functions of AtTIM22-2 in Arabidopsis remain poorly defined. Here, we report studies on two tim22-2 mutants that exhibit defects in embryo and endosperm development, leading to seed abortion. AtTIM22-2, which was localized in mitochondria, was widely expressed in embryos and in various seedling organs. Loss of AtTIM22-2 functions resulted in irregular mitochondrial cristae, decreased respiratory activity and a lower membrane potential, together with increased accumulation of reactive oxygen species (ROS), and in changes in gene expression and in enzyme activity related to ROS metabolism in the embryo. The levels of transcripts encoding mitochondrial protein import components were also changed in the tim22-2 mutants. Furthermore, mass spectrometry data, bimolecular fluorescence complementation and coimmunoprecipitation assays revealed that AtTIM22-2 interacted with AtTIM23-2, AtB14.7 and At5G27395. Taken together, these results demonstrate that AtTIM22-2 is essential for maintaining mitochondrial membrane functions during seed development. These findings lay the foundations for a new model for the composition and functions of the TIM22 complex in higher plants.