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        <identifier>oai:www.ideals.illinois.edu:2142/82525</identifier>
        <datestamp>2023-07-11</datestamp>
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          <dc:contributor>Stephanie Ceman</dc:contributor>
          <dc:creator>Ozawa, Rie</dc:creator>
          <dc:date>2015-09-25T20:45:40Z</dc:date>
          <dc:date>2015-09-25T20:45:40Z</dc:date>
          <dc:date>10000-01-01</dc:date>
          <dc:date>2008</dc:date>
          <dc:date>2008</dc:date>
          <dc:description>The X chromosome-linked form of Kallmann syndrome (KS) is caused by disruption of the Kal-1 gene, which encodes a secreted protein called Anosmin-1. The definitive features of the KS phenotype are anosmia and hypogonadism. Despite high conservation of the Kal-1 gene from invertebrates to vertebrates, the Kal-1 homolog in mice has not been identified. The unavailability of an animal model has hampered research on the disease  in vivo. Hence, little is known about the cellular processes and molecular functions underlying KS. Here, I isolated a Drosophila kal-1  null mutant, which removes the entire kal-1 coding region. Antibody staining shows that Anosmin-1 specifically localizes to the dendrites of olfactory receptor neurons (ORNs) throughout development. The dendrites of ORNs sense odorants in the environment including the  Drosophila melanogaster male-specific pheromone 11-cis-vaccenyl acetate, which is known to inhibit male-male mating behaviors. Interestingly, mutant males that lack kal-1 function inappropriately court other males. These results imply a possible role of kal-1 in mating behaviors in part by mediating pheromone perception.</dc:description>
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  Previous issue date: 2008</dc:description>
          <dc:description>Embargo set by: Seth Robbins for item 83806
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>92 p.</dc:description>
          <dc:description>Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2008.</dc:description>
          <dc:identifier>http://hdl.handle.net/2142/82525</dc:identifier>
          <dc:identifier>(MiAaPQ)AAI3347493</dc:identifier>
          <dc:language>eng</dc:language>
          <dc:subject>Biology, Neuroscience</dc:subject>
          <dc:title>Specific Roles of Kal-1 in Olfaction: A Model of Kallmann Syndrome in Drosophila</dc:title>
          <dc:type>text</dc:type>
          <degree>
            <department>Neuroscience</department>
            <discipline>Neuroscience</discipline>
            <grantor>University of Illinois at Urbana-Champaign</grantor>
            <level>Dissertation</level>
            <name>Ph.D.</name>
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