Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2023.07.31.551242v1?rss=1

Authors: Polina, I., Mishra, J., Cypress, M. W., Landherr, M., Valkov, N., Chaput, I., Nieto, B., Mende, U., Zhang, P., Jhun, B. S., O-Uchi, J.

Abstract:
MCU is widely recognized as a responsible gene for encoding a pore-forming subunit of highly mitochondrial-specific and Ca2+-selective channel, mitochondrial Ca2+ uniporter complex (mtCUC). Here, we report a novel short variant derived from the MCU gene (termed MCU-S) which lacks mitochondria-targeted sequence and forms a Ca2+-permeable channel outside of mitochondria. MCU-S was ubiquitously expressed in all cell-types/tissues, with particularly high expression in human platelets. MCU-S formed Ca2+ channels at the plasma membrane, which exhibited similar channel properties to those observed in mtCUC. MCU-S channels at the plasma membrane served as an additional Ca2+ influx pathway for platelet activation. Our finding is completely distinct from the originally reported MCU gene function and provides novel insights into the molecular basis of MCU variant-dependent cellular Ca2+ handling.

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