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eScholarship
Open Access Publications from the University of California

Scholarly Works (5 results)

  • Thesis
  • Peer Reviewed
UC Irvine Electronic Theses and Dissertations (2014)

Understanding the molecular mechanisms that govern animal development is one of the major challenges in developmental biology. The TGF-β members such as the bone morophogenetic proteins (BMP) play critical and diverse roles throughout embryonic development in both vertebrates and invertebrates and understanding the mechanisms by which they initiate specific cellular differentiation programs and control of gene expression is important. This dissertation will focus on the characterization of the BMP responsive element (BRE) identified in our lab. Additionally, I will demonstrate that the BRE functions as an activator in BRE-mediated BMP signaling and is responsible for modulating a subset of BMP target genes in mouse embryonic stem (ES) cells. To complement our in vitro studies, our lab also investigated the role of BMPs in early mouse embryonic development. Our studies reveal that BMP signaling may be active in the inner cell mass (ICM) during mouse embryogenesis and is playing a role in sustaining pluriopotency by interacting with the Oct4/Sox2/Nanog network.

    Cover page: The Regulation of BMP Signaling in Mouse Embryonic Stem Cells and Early Mouse Embryogenesis
    • Article
    • Peer Reviewed
    UC Irvine Previously Published Works (2012)
    • 1 supplemental ZIP
    Cover page: Bmp Indicator Mice Reveal Dynamic Regulation of Transcriptional ResponseCreative Commons 'BY' version 4.0 license
    • Article
    • Peer Reviewed
    UC Irvine Previously Published Works (2015)
    The mechanisms regulating cell division during development of the mouse pre-implantation embryo are poorly understood. We have investigated whether bone morphogenetic protein (BMP) signaling is involved in controlling cell cycle during mouse pre-implantation development. We mapped and quantitated the dynamic activities of BMP signaling through high-resolution immunofluorescence imaging combined with a 3D segmentation method. Immunostaining for phosphorylated Smad1/5/8 shows that BMP signaling is activated in mouse embryos as early as the 4-cell stage, and becomes spatially restricted by late blastocyst stage. Perturbation of BMP signaling in preimplantation mouse embryos, whether by treatment with a small molecule inhibitor, with Noggin protein, or by overexpression of a dominant-negative BMP receptor, indicates that BMPs regulate cell cleavage up to the morula stage. These results indicate that BMP signaling is active during mouse pre-implantation development and is required for cell cleavage in preimplantation mouse embryos.
      Cover page: BMP signaling is required for cell cleavage in preimplantation-mouse embryos.
      • Article
      • Peer Reviewed
      UC Irvine Previously Published Works (2015)
      The mechanisms regulating cell division during development of the mouse pre-implantation embryo are poorly understood. We have investigated whether bone morphogenetic protein (BMP) signaling is involved in controlling cell cycle during mouse pre-implantation development. We mapped and quantitated the dynamic activities of BMP signaling through high-resolution immunofluorescence imaging combined with a 3D segmentation method. Immunostaining for phosphorylated Smad1/5/8 shows that BMP signaling is activated in mouse embryos as early as the 4-cell stage, and becomes spatially restricted by late blastocyst stage. Perturbation of BMP signaling in preimplantation mouse embryos, whether by treatment with a small molecule inhibitor, with Noggin protein, or by overexpression of a dominant-negative BMP receptor, indicates that BMPs regulate cell cleavage up to the morula stage. These results indicate that BMP signaling is active during mouse pre-implantation development and is required for cell cleavage in preimplantation mouse embryos.
        Cover page: BMP signaling is required for cell cleavage in preimplantation-mouse embryos
        • Article
        • Peer Reviewed
        UCLA Previously Published Works (2011)
        Excessive or inappropriate activation of the immune system can be deleterious to the organism, warranting multiple molecular mechanisms to control and properly terminate immune responses. MicroRNAs (miRNAs), ∼22-nt-long noncoding RNAs, have recently emerged as key posttranscriptional regulators, controlling diverse biological processes, including responses to non-self. In this study, we examine the biological role of miR-146a using genetically engineered mice and show that targeted deletion of this gene, whose expression is strongly up-regulated after immune cell maturation and/or activation, results in several immune defects. Collectively, our findings suggest that miR-146a plays a key role as a molecular brake on inflammation, myeloid cell proliferation, and oncogenic transformation.
          Cover page: miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice
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