Project description:Expanding the exercise capacity is an emerging strategy to combat metabolic diseases. Skeletal muscle fiber type determination is critical for the exercise performance, but the regulatory basis is largely unknown. Here, we report that Sirt6 has a role in regulating myofiber configuration toward oxidative type and that Sirt6 activator can be an exercise mimetic. To elucidate molecular mechanisms, we performed RNA-sequencing analysis using WT and skeletal muscle-specific Sirt6 KO mice. Transcriptomic analysis enabled us to discover major signaling nodes altered by Sirt6 deficiency in close association with mitochondrial function and muscle phenotypes.
Project description:To understand the effects of Hsp60 deficiency in developing vertebrates, we generated CRISPR/Cas9-mediated hspd1 knockout zebrafish lines by targeting exon 2 to induce a frameshift mutation. We selected an allele with a 56 base pair deletion inducing a frameshift mutation leading to loss of protein functions. We examined the proteome changes in zebrafish larvae at 5 days post fertilization (DPF). Wildtype control and hspd1-/- larvae at 5dpf, were analyzed by TMT and nanoLC-MS/MS based proteomcis. For this purpose, we studied five pools from each genotype, and each pool consisted of five larvae.
Project description:Purpose: The transcriptional alterations underlying physiological changes in fetal alcohol spectrum disorder are largely unidentified. Here we perform RNA sequencing on 0% and 1% EtOH (12 hpf - 5 dpf) zebrafish at 7dpf stages in order to identify significant transcriptional alterations.
Project description:To understand the effects of Hsp60 deficiency in developing vertebrates, we generated CRISPR/Cas9-mediated hspd1 knockout zebrafish lines by targeting exon 2 to induce a frameshift mutation. We selected an allele with a 56 base pair deletion inducing a frameshift mutation leading to loss of protein functions. We examined the transcriptome changes in zebrafish larvae at 5 dpf .
Project description:As a member of class III histone deacetylases, Sirt6 has various functions including regulation of genomic stability, DNA repair, cancer, metabolism and ageing.Deficiency of Sirt6 is lethal and causes brain development redardation. We generated Emx1-cre induced Sirt6 conditional knockout mice model and found that Sirt6 deficiency promoted self-renew of neural precursor cells (NPCs) and inhibited differentiation. This result promotes understanding of the role of Sirt6 in brain development and NPCs’ fate determination and provides clues to explain the generality and difference between species.