10.5061/DRYAD.1B776V2
Stefanski, Heather E.
University of Minnesota
Xing, Yan
University of Minnesota
Taylor, Patricia A.
University of Minnesota
Maio, Stefano
University of Oxford
Henao-Meija, Jorge
University of Pennsylvania
Williams, Adam
Jackson Laboratory
Flavell, Richard A.
Yale University
Hollander, Georg A.
University of Oxford
University of Basel
Children's Hospital
Blazar, Bruce R.
University of Minnesota
Data from: Despite high levels of expression in thymic epithelial cells,
miR-181a1 and miR-181b1 are not required for thymic development
Dryad
dataset
2019
Thymus
thymic epithelial cells
Mus musculus
present
2019-07-02T00:00:00Z
2019-07-02T00:00:00Z
en
https://doi.org/10.1371/journal.pone.0198871
160564132 bytes
1
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
MicroRNAs (miRNAs) have been shown to be key modulators of
post-transcriptional gene silencing in many cellular processes. In
previous studies designed to understand the role of miRNAs in thymic
development, we globally deleted miRNA exclusively in thymic epithelial
cells (TECs), which are critical in thymic selection. This resulted in the
loss of stromal cells that instruct T cell lineage commitment and affect
thymocyte positive selection, required for mature T cell development.
Since murine miR-181 is expressed in the thymus and miR-181 deficiency
disrupts thymocyte development, we first quantified and thereby
demonstrated that miR181a1 and miR181b1 are expressed in purified TECs. By
generating mice with TEC targeted loss of miR-181a1 and miR-181b1
expression, we observed that neither TEC cellularity nor thymocyte number
nor differentiation was adversely affected. Thus, disrupted thymopoiesis
in miR-181 deficient mice was not due to miR-181 loss of expression in
TECs. Importantly, in mice with restricted TEC deficiency of miR-181a1 and
miR-181b1, there were similar numbers of mature T cells in the periphery
in regards to frequencies, differentiation, and function as compared to
controls. Moreover miR-181a1 and miR-181b1 were not required for
maintenance of thymus integrity over time, as thymic involution was not
accelerated in gene-targeted mice. Taken together our data indicate that
miR-181a1 and miR-181b1 are dispensable for TEC differentiation, their
control of thymocyte development and mature T cell export to and
homeostasis within the periphery.
Figure1Bmir181Figure1Bmir181Figure4Bmir181Figure4Bmir181Figure4Cmir181Figure4Cmir181Figure5A1mir181Figure5A1mir181Figure5Bmir181Figure5Bmir181FIgure5DMir181FIgure5DMir181Figure5Cmir181Figure2Band3mir181Figure2Band3mir181Figure 2a cre- mouseFigure 2a example FCS fileThy-A_Cre-neg #2_002.fcsFigure 2a cre positiveFigure 2a, exampleThy-A_Cre-pos #5_005.fcsTEC sort cre negative Figure 1aFigure 1aSpecimen_001-cre neg_10062016165112.pdfTEC sort Figure1a cre positiveFigure 1a cre+Specimen_001-cre pos_10062016165157.pdf
global