Project description:Gene expresion analysis among young mouse embryos, aging mouse embryos and aging mouse embryos suppressed their CXCL5-CXCR2 signaling.
Project description:Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos. Gene expression profiles between these two developmental stages identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.
Project description:We collected over 8000 mouse embryos of each developmental stage (zygote, 2-cell, 4-cell, 8-cell, morula, blastocyst) and performed tandem mass tag (TMT)-based quantitative mass spectrometry and identified nearly 5000 proteins for each stage. In-depth analysis indicates that protein expression profiles of zygote, morula and blastocyst show apparent difference from 2- to 8-cell embryos due to the maternal-totipotent-differentiation transition. We further identified novel factors and proved that they play important roles in determining pre-implantation embryo development
Project description:Transcriptional profiling of E9.5 mouse embryo tissue from the presomitic mesoderm (PSM) and somites I-IV. Tissue from embryos lacking a functional Paraxis gene (Paraxis-/-) was compared to identical tissue from E9.5 Wild Type embryos. The goal was to identify genes that had become deregulated in the absence of the transcription factor, Paraxis.
Project description:TRIM9 and TRIM67 are neuronally-enriched E3 ubiquitin ligases essential for neuronal morphogenesis and responses to the axon guidance cue netrin-1. Deletion of either gene in the mouse results in subtle neuroanatomical anomalies yet overt deficits in spatial learning and memory. The identify of few TRIM9 or TRIM67 substrates are known. Here we performed ubiquitin remnant profiling approach (Xu et al., 2010)in cultured cortical neurons from murine wildtype, Trim9-/-, Trim67-/-, and Trim9-/-:Trim67-/- embryos cultured with or without netrin-1 supplementation to attempt to identify proteins with altered ubiquitination. Although batch variability hindered our ability to identify differential protein ubiquitination, the results delineate the neuronal ubiquitionome during neurite outgrowth, axon specification, and axon branching.