MicroRNAs comprise 1-3% of all vertebrate genes, but their in vivo functions and mechanisms of action remain largely unknown. Zebrafish miR-430 is expressed at the onset of zygotic transcription and regulates morphogenesis during early development. Using a microarray approach and in vivo target validation, we find that miR-430 directly regulates several hundred target mRNAs. Targets are highly enriched for maternal mRNAs that accumulate in the absence of miR-430. We also show that miR-430 accelerates the deadenylation of target mRNAs. These results suggest that miR-430 facilitates the deadenylation and clearance of maternal mRNAs during early embryogenesis.
Zebrafish MiR-430 promotes deadenylation and clearance of maternal mRNAs.
No sample metadata fieldsView Samples
The aim of this study was to identify the transcriptomic response 6 hours after the MRT irradiation, in normal brain tissue (11 samples) and in glioma tissue (11 samples), in rat.
Early gene expression analysis in 9L orthotopic tumor-bearing rats identifies immune modulation in molecular response to synchrotron microbeam radiation therapy.
Specimen partView Samples
Several studies indicate that SMN-containing mRNP complexes could be involved in the axonal localization of a large number of mRNAs. We have used murine motor neuron-like NSC-34 cells and RNA Immuno-Precipitation experiments coupled to microarray analyses to perform a genome-wide analysis of RNA species present in mRNP complexes containing the full length SMN protein (flSMN). In situ hybridization and immuno-fluorescence experiments performed on several candidates indicate that these mRNAs colocalize with the SMN protein in neurites and axons of differentiated NSC-34 cells. Moreover, they localize in cell processes in a SMN-dependent manner. Thus, low SMN levels might result in localization deficiencies of mRNAs required for axonogenesis.
Genome-wide identification of mRNAs associated with the protein SMN whose depletion decreases their axonal localization.
Specimen part, Cell lineView Samples
Classical dendritic cells (cDCs) process and present antigens to T cells. Under steady-state conditions, antigen presentation by cDCs induces tolerance. In contrast, during infection or inflammation, cDCs become activated, express higher levels of cell surface MHC molecules, and induce strong adaptive immune responses. We recently identified a cDC-restricted zinc finger transcription factor, zDC, that is not expressed by other immune cell populations, including pDCs, monocytes, or macrophages. Here we define the zDC consensus DNA binding motif and the genes regulated by zDC using chromatin immunoprecipitation and deep sequencing. By deleting zDC from the mouse genome, we show that zDC is primarily a negative regulator of cDC gene expression. zDC deficiency alters the cDC subset composition in the spleen in favor of CD8+ DCs, upregulates activation pathways in steady state cDCs including elevated MHC II expression, and enhances cDC production of VEGF leading to increased vascularization of skin-draining lymph nodes. Consistent with these observations, zDC protein expression is rapidly downregulated after TLR ligation. Thus, zDC is a TLR-responsive cDC-specific transcriptional repressor that is in part responsible for preventing cDC maturation in the steady state.
Zinc finger transcription factor zDC is a negative regulator required to prevent activation of classical dendritic cells in the steady state.
Sex, Specimen partView Samples