SAT-013 C-MSI1, a Novel Musashi Isoform and Driver of Embryonic Pluripotency is Expressed in the Adult Pituitary

Abstract Disclosure: C.R. Bolen: None. M.M. Reddick: None. L. Hardy: None. D. Alkam: None. S. Byrum: None. A. Herdman: None. A. Lagasse: None. A.K. Odle: None. G.V. Childs: None. M.C. MacNicol: None. K.K. Stephens: None. A.M. MacNicol: None. The mRNA translation control protein, Musashi (MSI), plays a critical role in mediating physiological and pathological stem cell function in many tissue types. A novel truncated isoform of MSI1 (C-MSI1) has been recently described in mouse and human embryonic stem cells (ESCs) that encodes the C-terminal portion of the MSI1 protein and lacks the conserved RNA-recognition domains. The C-MSI1 protein was shown to be nuclear, to persist in current mouse Msi1 deletion models and to be required for embryonic stem cell pluripotency. We have previously reported that MSI is expressed in the adult anterior pituitary stem cells but surprisingly, is also broadly expressed in non-stem/progenitor cell populations where it appears to modulate hormone expression. Our new data demonstrate that C-MSI1 is also abundant in the adult pituitary, with C-Msi1 expression driven through a promoter residing within intron 6 of the full-length mouse Msi1 gene. The role of C-MSI1 in modulation of hormone-producing cell lineage specification and the unique partner proteins with which it acts are the focus of this study. These analyses will elucidate the regulation and role of the newly discovered C-MSI1 isoform with regard to pituitary stem cell function and control of adult pituitary hormone expression. Presentation: Saturday, July 12, 2025