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        <identifier>oai:www.ideals.illinois.edu:2142/86327</identifier>
        <datestamp>2023-07-11</datestamp>
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          <dc:contributor>Henry, Jonathan J.</dc:contributor>
          <dc:creator>Barsoum, Ivraym Boshra</dc:creator>
          <dc:date>2015-09-28T15:03:21Z</dc:date>
          <dc:date>2015-09-28T15:03:21Z</dc:date>
          <dc:date>10000-01-01</dc:date>
          <dc:date>2009</dc:date>
          <dc:date>2009</dc:date>
          <dc:description>"The main hypothesis of this dissertation was that gonadal Hh signaling, through the putative mammalian GLI proteins, is alone essential and sufficient to induce FLC differentiation. My objective was to address three main questions concerning the role of Hh signaling in gonadal development. In chapter III, I addressed the first question on whether Hh signaling is sufficient to induce FLC differentiation. Indeed, Hh activation led to appearance of ectopic functional FLCs in the ovary. In  chapter IV, I addressed the second question on the essential role of GLI and GLI2, as Hh transcriptional activators, to induce FLC development. My data showed that both GLI1 and GLI2 were modulators of Hh to establish FLCs. In chapter V, I addressed the third question on the possible role of GLI3 (as a transcriptional repressor) to silence the Hh pathway in the fetal ovary, which expresses other mammalian Hh genes, such as Shh. The repressor form of GLI3 was expressed in the fetal ovary, and null mutation of Gli3 led to Hh activation and steroidogenic cell appearance. In chapter VI, I used the Hh signaling over-activation as a tool to identify the progenitors of FLCs in the mouse fetal testis. In the appendix, I compiled the data that are not included in chapters III to VI. In the ""future directions"" section, I provided speculations and ways to further investigate the questions that have been raised though the course my research."</dc:description>
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  Previous issue date: 2009</dc:description>
          <dc:description>Embargo set by: Seth Robbins for item 87608
Lift date: Forever
Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs</dc:description>
          <dc:description>Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs</dc:description>
          <dc:description>U of I Only</dc:description>
          <dc:description>148 p.</dc:description>
          <dc:description>Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2009.</dc:description>
          <dc:identifier>http://hdl.handle.net/2142/86327</dc:identifier>
          <dc:identifier>(MiAaPQ)AAI3391882</dc:identifier>
          <dc:language>eng</dc:language>
          <dc:subject>Biology, Molecular</dc:subject>
          <dc:title>Dissecting the Role of Hedgehog Pathway in Murine Gonadal Development</dc:title>
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            <department>Cell and Developmental Biology</department>
            <discipline>Cell and Developmental Biology</discipline>
            <grantor>University of Illinois at Urbana-Champaign</grantor>
            <level>Dissertation</level>
            <name>Ph.D.</name>
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