These studies reveal that BMPR2 signaling regulates TAK1-d splice variant to mediate mitochondrial Ca2+ transport, which is dependent on the MCU. Our studies suggest that BMPR2 signaling utilizes mtCa2+ transport to regulate both mitochondrial bioenergetics and/or cell survival. Our studies provide novel insight into how aberrant BMPR2 signaling is pathogenic and suggests that the response could vary depending on the cell type.
Toussaint et al. (Wed,) studied this question.