PRELID1, the only late embryogenesis abundant (LEA) domain-containing protein in humans, is a lipid transfer protein in the Ups/PRELI family. It facilitates the transport of phosphatidic acid (PA) across the mitochondrial intermembrane space, which is crucial for the conversion of PA to cardiolipin (CL), a signature phospholipid of mitochondria. This process is essential for maintaining mitochondrial structure and function. PRELID1 also plays roles in stress response and is associated with pathways like the unfolded protein response (UPR) and mTORC1 signaling [3,4,5].

In breast cancer, an alternative polyadenylation (APA) event in PRELID1 mRNA enhances its steady-state level and translational efficiency, and is a strong breast-cancer-subtype-dependent predictor of patient clinical outcomes. PRELID1 also regulates stress response and mitochondrial reactive oxygen species (ROS) production in a cell-type-specific manner. In mesenchymal stem cell-treated thymic epithelial cells, decreased methylation of PRELID1 promoter leads to its up-regulation, promoting cell growth [1,2]. In yeast lacking Ups1 (a homolog of PRELID1), disturbed intramitochondrial PA transport impairs glycolytic growth and cellular stress signaling, such as UPR and mTORC1 signaling [3].

In summary, PRELID1 is vital for mitochondrial lipid transport and stress-related cellular functions. Its study, especially through model-based research like in yeast models similar to Ups1-deficient yeast, has revealed its significance in cancer and cell growth-related disease areas. In cancer, it is associated with patient outcomes and mitochondrial ROS signaling, while in thymus aging, it is involved in the regulation of cell growth through DNA methylation-related mechanisms [1,2,3].