Project description:In the mouse neocortex, neural progenitor cells generate neurons through repeated rounds of asymmetric cell division. How distinct fates are established in their daughter cells is unclear. We show here that the TRIM-NHL protein TRIM32 segregates asymmetrically during progenitor division and induces neuronal differentiation in one of the two daughter cells. TRIM32 is highly expressed in differentiating neurons. In both horizontally and vertically dividing progenitor cells, TRIM32 distribution becomes polarized in mitosis so that the protein is enriched in one of the two daughter cells. While TRIM32 overexpression induces cell cycle exit and neuronal differentiation, TRIM32 RNAi causes both daughter cells to proliferate and prevents the initiation of a neuronal differentiation program . TRIM32 ubiquitinates and degrades the transcription factor c-Myc but also binds Argonaute-1 and thereby increases the activity of specific micro-RNAs. We show that Let-7 is one of the TRIM32 targets and is required and sufficient for neuronal differentiation. Our data suggest that the asymmetric segregation of a micro RNA regulator controls self renewal in the mammalian brain. Experiment Overall Design: small RNA from total mouse brain, Ago-1 and TRIM32 IPs were cloned and sequenced using 454 GS FLX system.
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:Small RNAs are emerging as important molecules for cross-species communication. Thanks to available and affordable sequencing technologies it is now possible to sequence small RNAs (sRNA-Seq) present in samples of interacting organisms. A first step when analyzing sRNA-Seq of two interacting species is to determine which sequences are being produced by which organism. Due to their small size (18-30), small RNAs could easily map to both host and parasite genomes. Here we produced data for Mus musculus intestinal epithelial cells treated with Extracellular Vesicles (EV) produced by the parasitic nematode Heligmosomoides bakeri.
Project description:In the mouse neocortex, neural progenitor cells generate neurons through repeated rounds of asymmetric cell division. How distinct fates are established in their daughter cells is unclear. We show here that the TRIM-NHL protein TRIM32 segregates asymmetrically during progenitor division and induces neuronal differentiation in one of the two daughter cells. TRIM32 is highly expressed in differentiating neurons. In both horizontally and vertically dividing progenitor cells, TRIM32 distribution becomes polarized in mitosis so that the protein is enriched in one of the two daughter cells. While TRIM32 overexpression induces cell cycle exit and neuronal differentiation, TRIM32 RNAi causes both daughter cells to proliferate and prevents the initiation of a neuronal differentiation program . TRIM32 ubiquitinates and degrades the transcription factor c-Myc but also binds Argonaute-1 and thereby increases the activity of specific micro-RNAs. We show that Let-7 is one of the TRIM32 targets and is required and sufficient for neuronal differentiation. Our data suggest that the asymmetric segregation of a micro RNA regulator controls self renewal in the mammalian brain.