Area:
Genetics, Neuroscience Biology, Cell Biology, Pathology
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High-probability grants
According to our matching algorithm, Michael J. Jurynec is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2002 — 2004 |
Jurynec, Michael J |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Zebrafish Neural Crest Induction and Proliferation
DESCRIPTION (provided by applicant): Neural crest (NC) cells are an embryonic, multipotent population of stem cells that arise from the lateral edges of the neural plate. Once the neural plate has formed the neural tube, NC migrate away from the dorsal neural tube to contribute to a wide variety of neuronal and non-neuronal tissues, including cells of the heart, peripheral nervous system, enteric nervous system, craniofacial cartilage, and pigmented cells. The proposed studies are aimed at understanding the processes that govern the establishment of the premigratory NC population in the zebrafish (Danio rerio). This is important because mutations that reduce the number of premigratory NC have defects in formation of differentiated tissues (e.g., the splotch/pax-3 mouse mutant). Also perturbations in NC development are a major component of human congenital syndromes involving craniofacial, heart, and enteric nervous system development. The generation of premigratory NC has been proposed to be a multistep process involving induction of a precursor population followed by its proliferative expansion. Bone morphogenetic proteins (Bmps), fibroblast growth factors (Fgfs), and Wnts are growth factors important for generating the final number of premigratory NC population. However, their precise roles in the processes of early NC induction and proliferation are not well understood. I will combine experimental embryology with genetic manipulations in the zebrafish to 1. establish assays that differentiate between induction and proliferation of early NC cells 2. test whether Bmps, Fgf, and Wnts affect induction and/or proliferation, and 3. characterize the role and identity of a new gene, alyron (aln) that is required for the generating the premigratory NC population.
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1 |
2020 — 2021 |
Grunwald, David J. [⬀] Jurynec, Michael J |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Establishing a New Genetic Mouse Model of Osteoarthritis
Osteoarthritis (OA) is the major cause of disability among the aging, affecting more than 30 million adults in the US. It is a painful and debilitating disease involving abnormal remodeling of joint tissues. No cure for OA exists and surgical intervention is the only effective therapy. No known treatment prevents initiation or progression of the disease. Lack of understanding of the genes, molecular pathways, and biological processes underlying susceptibility to OA is the key limitation to the development of effective therapies. As noted in the FOA (16- 240) to which this proposal responds: ?little is understood about the initial changes triggering disease etiology and early progression.? Our goal is to identify molecular pathways that are vulnerability points for the development of OA: We first discover human gene variants associated with susceptibility to OA and then determine whether and how these gene variants confer susceptibility to OA in genetically modified mouse models. We predict the pathways perturbed by these alleles are pathways whose normal functions guard against OA. We hypothesize these are the pathways that are eroded or compromised during aging. We have identified four families that harbor strongly supported OA-susceptibility variants in genes encoding components of the NOD-RIPK2 signaling pathway. This pathway uses NOD pattern recognition receptors to sense breakdown products and promote inflammatory signaling that directs tissue homeostasis. We propose modulation of NOD-RIPK2 signaling can contribute to OA susceptibility. In this proposal we test whether a rare RIPK2 variant, which segregates with OA and is hyperactive in signaling, affects normal physiology and/or joint maintenance in mice and is sufficient to confer susceptibility to OA in mice. We generated a precisely modified C57Bl/6 mouse that carries the variant protein-coding allele. In two aims we will test if the variant RIPK2104Asp allele: 1) causes an aberrantly prolonged or sustained inflammatory response; 2) alters maintenance of the joint in naturally aging mice; and 3) enhances the onset and/or severity of OA initiated by mechanical injury to the knee joint. The scientific premise for study of the mouse model is strong. The RIPK2 allele segregates as a highly penetrant dominant factor linked to OA and the OA-associated RIPK2 product has increased signaling activity relative to the wildtype protein. Recently we demonstrated the single amino acid substitution has a measurable effect on the immune response of B6 mice. We hypothesize the RIPK2 variant acts as a gain- of-function allele to over-stimulate the inflammatory response to naturally occurring or induced joint damage. Our studies will determine if the RIPK2 allele is sufficient to increase susceptibility to OA in mice, begin to test the link between the NOD-RIPK2 inflammation pathway and OA, and determine types of initiating events that trigger this pathway. Having a mouse model of an allele linked to a common, idiopathic form of OA will allow us in the future to identify i) specific cell types and biological pathways that are key to vulnerability to OA and ii) additional factors that interact with and exacerbate the effect of RIPK2 signaling on OA.
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