Data from: Musashi exerts control of gonadotrope target mRNA translation during the mouse estrous cycle

The anterior pituitary controls key biological processes, including
growth, metabolism, reproduction and stress responses through distinct
cell types that each secrete specific hormones. The anterior pituitary
cells show a remarkable level of cell type plasticity that mediates the
shifts in hormone producing cell populations that are required to meet
organismal needs. The molecular mechanisms underlying pituitary cell
plasticity are not well understood. Recent work has implicated the
pituitary stem cell populations and specifically, the mRNA binding
proteins of the Musashi family in control of pituitary cell type identity.
In this study we have identified the target mRNAs that mediate Musashi
function in the adult mouse pituitary and demonstrate the requirement for
Musashi function in vivo. Using Musashi RNA immunoprecipitation, we
identify a cohort of 1184 mRNAs that show specific Musashi binding.
Identified Musashi targets include the Gnrhr mRNA, which encodes the
gonadotropin releasing hormone receptor (GnRHR), and the Fshb mRNA,
encoding follicle-stimulating hormone (FSH). Reporter assays reveal that
Musashi functions to exert repression of translation of the Fshb mRNA, in
addition to the previously observed repression of the GnrhrmRNA.
Importantly, mice engineered to lack Musashi in gonadotropes demonstrate a
failure to repress translation of the endogenous Gnrhr and Fshb mRNAs
during the estrous cycle and display a significant heterogeneity in litter
sizes. The range of identified target mRNAs suggests that, in addition to
these key gonadotrope proteins, Musashi may exert broad regulatory control
over the pituitary proteome in a cell-type specific manner.