DOI: 10.5061/dryad.bcc2fqzfj
title: Data from: Musashi exerts control of gonadotrope target mRNA translation during the mouse estrous cycle

description: 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.
description: Author generated RNA sequencing data (see Gene Expression Omnibus
 (GEO) under accession number GSE199098) with differential mRNA enrichment
 in Musashi vs control IgG immunoprecipitation performed as described in
 primary manuscript.   Supp. Figure S1- additional
 bioinformatic analyses and western blot performed as described in
 accompanying supplementary figure legends.  Supp.
 Figure S2 - validation of mouse genotypes Supp. Figure
 S3 - additional charaacterization of mouse gonadotropin levels, mRNA and
 protein Supplemental Tables 1-7 - include all recovered
 mRNAs (Supp. Table 1); mRNAs enriched in Musashi1/2 over IgG control
 immunoprecipitations log2FC&gt;1 and adj P &lt;0.1 (Supp. Table
 2); mRNA enriched in Musashi immunoprecipitations apparently lacking MBEs
 (Supp. Table 3); pituitary lineage-restricted Musashi target mRNAs (Supp.
 Table 4); ; Musashi target mRNA comaprison to other published studies
 (Supp. Table 5); and GO analysis of mRNAs common to Msi1 or MSi2 across
 species and tissue types (Supp. Table 6).
description: Data files can be accessed using Word, Excel and Powerpoint.
description: # The cell fate determinant Musashi acts as a post-transcriptional
 regulator in the pituitary: Implications for control of gonadotrope
 function 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 Gnrhr mRNA.
 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 abberant ovarian follicle
 developement. 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. ## Description of the data and file structure This supplemental
 data set includes supporting figures and Tables as cited in the primary
 manuscript. These include Author generated RNA sequencing data (see Gene
 Expression Omnibus (GEO) under accession number GSE199098) with
 differential mRNA enrichment in Musashi vs control IgG immunoprecipitation
 performed as described in primary manuscript. Supp. Figure S1- additional
 bioinformatic analyses performed as described in accompanying
 supplementary figure legends. Supp. Figure S2 - validation of mouse
 genotypes Supp. Figure S3 - additional charaacterization of mouse
 gonadotropin levels, mRNA and protein Supplemental Tables 1-7 - include
 all recovered mRNAs (Supp. Table 1); mRNAs enriched in Musashi1/2 over IgG
 control immunoprecipitations log2FC&gt;1 and adj P &lt;0.1 (Supp. Table
 2); mRNA enriched in Musashi immunoprecipitations apparently lacking MBEs
 (Supp. Table 3); pituitary lineage-restricted Musashi target mRNAs (Supp.
 Table 4); ; Musashi target mRNA comaprison to other published studies
 (Supp. Table 5); and GO analysis of mRNAs common to Msi1 or MSi2 across
 species and tissue types (Supp. Table 6). FIgures require powerpoint,
 Tables require Excel and text documents require WORD top open ##
 Sharing/Access information: All data is freely accessable via Dryad