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High-probability grants
According to our matching algorithm, Mark Zervas is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2003 — 2005 |
Zervas, Mark |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Lineage &Development of the Midbrain &Hindbrain @ New York University School of Medicine
DESCRIPTION (provided by applicant): The vertebrate brain is derived from the rostral neural tube, which first appears as a series of morphological constrictions termed neuromeres that delineate the major subdivisions of the brain. Tissue specific patterning of neuromeres results in highly specialized anatomical and functional units in the adult. One method to accomplish these remarkable developmental events is with a combinatorial mechanism of patterning that involves the formation of a lineage restriction boundary concomitant with the emergence of an 'organizer' that instructs specific positional information and fates on adjacent tissue. This mechanism has been shown to pattern Drosophila wing imaginal disks as well as chick and mouse limb but not as of yet brain. The mesencephalon (mes) and metencephalon (met) are opposed to each other and are clearly distinct morphological structures. During early development the mes, which expresses Otx2 and Wnt1, and the met, which expresses Gbx2 and Fgf8, are juxtaposed at a well-defined constriction along the anteroposterior axis defined as the isthmus. The differentially expressed mes/met genes specify regional identity and potentially segregate two populations of cells into presumptive compartments. Interestingly, the isthmus has been shown to be an organizer using classical transplantation studies and appears to mediate instructional events through a complex genetic cascade initiated by the morphogen Fgf8. The secreted factor Wnt1 may play a role in maintaining mes/met boundary integrity, though this mechanism has not been closely studied. This proposal will investigate whether the mes/met juxtaposition is a lineage restriction boundary and addresses the role of Wnt1 in mes/met boundary formation or maintenance. I propose to address these questions by genetically marking and fate mapping Wnt1 expressing cells of the mes and Gbx2-expressing cells of the met using two inducible Cre/loxP systems. To address whether Wnt1 plays a role in establishing and/or maintaining the mes/met interface, I will generate a conditional Wnt1 mutant allele and assess the phenotypic consequences of loss of Wnt1 function at different developmental stages.
|
0.966 |
2011 |
Zervas, Mark |
P20Activity Code Description: To support planning for new programs, expansion or modification of existing resources, and feasibility studies to explore various approaches to the development of interdisciplinary programs that offer potential solutions to problems of special significance to the mission of the NIH. These exploratory studies may lead to specialized or comprehensive centers. |
Determining the Transcriptional Regulation &Cell Signaling Events That Shape Th
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. A diverse array of neurons is essential for mammalian nervous system function. It is well known that the loss or dysfunction of specific subsets of neurons causes distinct neurological disorders. Parkinson's disease which has a devastating and negative impact on human health is the result of the degeneration of midbrain dopamine neurons of the substantia nigra, which are positioned in the lateral midbrain. The loss of substantia nigra dopamine neurons results in the inability to properly control movement. A current line of treatment proposed to treat Parkinson's disease is to use embryonic stem cell or induced pluripotent stem cell based therapy. The fundamental concept using cell based therapies is to transplant dopamine neuron precursors into patients with Parkinson's disease. A surrogate to test these approaches is transplant dopamine neuron precursors into animal models with midbrain dopamine neuron loss. However, a significant knowledge gap is that we do not understand how substantia nigra neurons are established during mammalian development, which translates into a problem of how to make the appropriate type of dopamine neuron. These deficits need to be addressed to design effective cell-based therapies to treat neurodegenerative diseases like Parkinson's disease. Currently there is no protocol to effectively instruct stem cells to acquire the most appropriate fate to ameliorate MbDA neuron-specific diseases. We have identified the dopamine neuron progenitor pool in vivo and determined that these progenitors express the gene Wnt1 during multiple critical steps for dopamine neuron development. The purpose of this proposal is to establish the molecular identity of Wnt1-expressing progenitors that contribute to developing dopamine neurons and to identify how WNT signaling specifies MbDA neuron progenitors. The studies in this proposal forge a link between the concept of cell fate specification and the problem of how distinct neuronal subtypes are established. An expected outcome is that we will elucidate regulatory components used to control the development of MbDA neuron subtypes from a complex progenitor pool. The positive impact of this application is that by uncovering how subtypes are allocated, we will provide a molecular scaffold that can be exploited to effectively guide stem cells to acquire a unique MbDA identity.
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0.883 |