MiRNA sequencing of Trim71 conditional ("WT") and Trim71 KO mES cells
Ontology highlight
ABSTRACT: We report that Trim71 mutation induces significant changes in the global expression profile of miRNAs in undifferentiated mES cells, rendering the cells prone to differentiation.
Project description:We report that Trim71 mutation does not lead to significant changes within the core regulatory network of mES cells, however, there is an upregulation of specific genes involved in neural differentiation. We thus conclude that Trim71 KO mES cells are poised for differentiation.
Project description:We studies on Trim71 regulates mouse embryonic stem cells by identifying the transcriptome-wide RNA targets of Trim71. Moreover, through inhibiting specific Trim71:mRNA interactions, we determined how Trim71 modulate miRNA activity in mouse embryonis cell cells
Project description:Mutations in TRIM71’s RNA-binding domain leads to congenital hydrocephalus in human patients and a TRIM71 mutant mouse model (Trim71R595H/+). Additionally, homozygous Trim71R595H/R595H mice phenocopy the neural tube defects and premature neural differentiation observed in TRIM71-KO mice. As RNA-Seq analyses revealed that TRIM71-KO mESC are poised for neural differentiation, we aimed to also examine the transcriptomes of TRIM71R595H/R595H and TRIM71R595H/+ mESC. Both TRIM71-KO and TRIM71R595H/R595H mutations in mESC result in transcriptomic changes with similar patterns, when compared to control mESC. Similar to TRIM71-KO, the transcriptome of Trim71R595H/R595H mESC indicates a poised state of mutated mESC towards neural differentiation.
Project description:During embryonic development in mice, global deficiency of Trim71 (Trim71-KO) leads to defects in vascular development of the yolk sac and impaired primitive erythropoiesis. These phenotypes start to become apparent at E9.5. We analyzed changes in gene expression by single-cell RNA-sequencing (scRNA-seq) in whole Trim71-KO embryos compared to wildtype embryos at an early developmental stage (E7.5, late gastrulation) to investigate the onset of these phenotypes. Furthermore, we analyzed Trim71-KO and wildtype yolk sacs at E9.5 by scRNA-seq to gain insight into the changes in gene expression at the developmental stage when vascular defects have become apparent.
Project description:We demonstrate that global effects of TRIM71 on the cellular transcriptome of mouse embryonic stem cells (mESCs) are largely attributable to its RNA binding activity, and map the transcriptome-wide targets of wild-type TRIM71, NHL domain mutant TRIM71, and RING domain mutant TRIM71.
Project description:We identify mammalian TRIM71 as repressor of mRNAs that inhibits translation and affects mRNA stability. In this data set we compare the expression profile of mouse ES upon Trim71 KD versus that of the parental cells. Experiment was performed in triplicate.