Data from: Despite high levels of expression in thymic epithelial cells, miR-181a1 and miR-181b1 are not required for thymic development

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.