{"id":{"repo_id":"cuny","oai_identifier":"oai:academicworks.cuny.edu:cc_etds_theses-1840"},"canonical_url":"https://search.dev.ndltd.org/etd/cuny/oai:academicworks.cuny.edu:cc_etds_theses-1840","repository":{"repo_id":"cuny","name":"City University of New York - City College","base_url":"https://academicworks.cuny.edu/do/oai/"},"display":{"title":"Role of MOA-1, an Anti-phosphatase, and APL-1, an APP-related Protein, in Morphogenesis and Mating Behavior in Caenorhabditis elegans","abstract":"<p>Alzheimer's disease is a neurodegenerative disease that affects more than 30 million people globally. The disease is characterized by an accumulation of extracellular beta-amyloid peptide plaques and intracellular neurofibrillary tangles in the brain. The beta-amyloid peptide is derived from a larger precursor protein, the amyloid precursor protein (APP). Mutations in APP have been correlated with Alzheimer's disease. Due to the presence of two paralogues, APLP1 and APLP2, which have overlapping functions, the normal function of APP is difficult to elucidate. Knockout of the entire APP gene family in mice results in lethality and developmental defects, indicating that the APP gene family has an essential function. The nematode Caenorhabditis elegans has one APP ortholog,<em> apl-1</em>. <em>apl-1</em>(yn10) knockouts are not viable, indicating that <em>apl-1</em> has an essential function. <em>apl-1</em>(yn5) is a temperature sensitive allele; these mutants produce only the extracellular domain of APL-1. At the permissive temperature <em>apl-1</em>(yn5) mutants have many phenotypic defects, which include poor mating and delayed development; at the restrictive temperature, <em>apl-1</em>(yn5) mutants show an incompletely penetrant lethality. moa-1 mutations suppress the<em> apl-1</em>(yn5) lethality at the restrictive temperature. Surprisingly, <em>moa-1</em> is involved in male tail development; the male tail is critical for successful mating. This project focused on studying the morphology and mating behavior of yn5 mutants, <em>moa-1</em> transgenic animals, and other mutants regulating male tail development. Strains were characterized for morphology and mating behavior without knowledge of the genotype of the animals. Understanding male tail development may provide insights into other pathways in which <em>apl-1</em> functions.</p>","abstract_html":"&lt;p&gt;Alzheimer&#x27;s disease is a neurodegenerative disease that affects more than 30 million people globally. The disease is characterized by an accumulation of extracellular beta-amyloid peptide plaques and intracellular neurofibrillary tangles in the brain. The beta-amyloid peptide is derived from a larger precursor protein, the amyloid precursor protein (APP). Mutations in APP have been correlated with Alzheimer&#x27;s disease. Due to the presence of two paralogues, APLP1 and APLP2, which have overlapping functions, the normal function of APP is difficult to elucidate. Knockout of the entire APP gene family in mice results in lethality and developmental defects, indicating that the APP gene family has an essential function. The nematode Caenorhabditis elegans has one APP ortholog,&lt;em&gt; apl-1&lt;/em&gt;. &lt;em&gt;apl-1&lt;/em&gt;(yn10) knockouts are not viable, indicating that &lt;em&gt;apl-1&lt;/em&gt; has an essential function. &lt;em&gt;apl-1&lt;/em&gt;(yn5) is a temperature sensitive allele; these mutants produce only the extracellular domain of APL-1. At the permissive temperature &lt;em&gt;apl-1&lt;/em&gt;(yn5) mutants have many phenotypic defects, which include poor mating and delayed development; at the restrictive temperature, &lt;em&gt;apl-1&lt;/em&gt;(yn5) mutants show an incompletely penetrant lethality. moa-1 mutations suppress the&lt;em&gt; apl-1&lt;/em&gt;(yn5) lethality at the restrictive temperature. Surprisingly, &lt;em&gt;moa-1&lt;/em&gt; is involved in male tail development; the male tail is critical for successful mating. This project focused on studying the morphology and mating behavior of yn5 mutants, &lt;em&gt;moa-1&lt;/em&gt; transgenic animals, and other mutants regulating male tail development. Strains were characterized for morphology and mating behavior without knowledge of the genotype of the animals. Understanding male tail development may provide insights into other pathways in which &lt;em&gt;apl-1&lt;/em&gt; functions.&lt;/p&gt;","abstract_has_math":false,"creators":["Moscoso, Valerie C"],"institution":null,"degree_name":"Master of Science (M.S.)","degree_level":"Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Chrsitine Li","Jonathan Levitt","Itzhek Mano"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-01-01T08:00:00Z","date_published":"2019-01-01T08:00:00Z","updated_at":"2026-07-24T01:57:21Z","subjects":["male tail morphogenesis nematode alzheimer's mating","Biology","Genetics and Genomics"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://academicworks.cuny.edu/cc_etds_theses/780","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Chrsitine Li","Jonathan Levitt","Itzhek Mano"]},{"key":"dc:creator","label":"Author","values":["Moscoso, Valerie C"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2024-06-03T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (M.S.)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["male tail morphogenesis nematode alzheimer's mating","Biology","Genetics and Genomics"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://academicworks.cuny.edu/cc_etds_theses/780"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["<p>Alzheimer's disease is a neurodegenerative disease that affects more than 30 million people globally. The disease is characterized by an accumulation of extracellular beta-amyloid peptide plaques and intracellular neurofibrillary tangles in the brain. The beta-amyloid peptide is derived from a larger precursor protein, the amyloid precursor protein (APP). Mutations in APP have been correlated with Alzheimer's disease. Due to the presence of two paralogues, APLP1 and APLP2, which have overlapping functions, the normal function of APP is difficult to elucidate. Knockout of the entire APP gene family in mice results in lethality and developmental defects, indicating that the APP gene family has an essential function. The nematode Caenorhabditis elegans has one APP ortholog,<em> apl-1</em>. <em>apl-1</em>(yn10) knockouts are not viable, indicating that <em>apl-1</em> has an essential function. <em>apl-1</em>(yn5) is a temperature sensitive allele; these mutants produce only the extracellular domain of APL-1. At the permissive temperature <em>apl-1</em>(yn5) mutants have many phenotypic defects, which include poor mating and delayed development; at the restrictive temperature, <em>apl-1</em>(yn5) mutants show an incompletely penetrant lethality. moa-1 mutations suppress the<em> apl-1</em>(yn5) lethality at the restrictive temperature. Surprisingly, <em>moa-1</em> is involved in male tail development; the male tail is critical for successful mating. This project focused on studying the morphology and mating behavior of yn5 mutants, <em>moa-1</em> transgenic animals, and other mutants regulating male tail development. Strains were characterized for morphology and mating behavior without knowledge of the genotype of the animals. Understanding male tail development may provide insights into other pathways in which <em>apl-1</em> functions.</p>"]},{"key":"dc:title","label":"Title","values":["Role of MOA-1, an Anti-phosphatase, and APL-1, an APP-related Protein, in Morphogenesis and Mating Behavior in Caenorhabditis elegans"]}]}],"canonical_facts":{"dc:contributor":["Chrsitine Li","Jonathan Levitt","Itzhek Mano"],"dc:creator":["Moscoso, Valerie C"],"dc:date.available":["2024-06-03T07:00:00Z"],"dc:description.abstract":["<p>Alzheimer's disease is a neurodegenerative disease that affects more than 30 million people globally. The disease is characterized by an accumulation of extracellular beta-amyloid peptide plaques and intracellular neurofibrillary tangles in the brain. The beta-amyloid peptide is derived from a larger precursor protein, the amyloid precursor protein (APP). Mutations in APP have been correlated with Alzheimer's disease. Due to the presence of two paralogues, APLP1 and APLP2, which have overlapping functions, the normal function of APP is difficult to elucidate. Knockout of the entire APP gene family in mice results in lethality and developmental defects, indicating that the APP gene family has an essential function. The nematode Caenorhabditis elegans has one APP ortholog,<em> apl-1</em>. <em>apl-1</em>(yn10) knockouts are not viable, indicating that <em>apl-1</em> has an essential function. <em>apl-1</em>(yn5) is a temperature sensitive allele; these mutants produce only the extracellular domain of APL-1. At the permissive temperature <em>apl-1</em>(yn5) mutants have many phenotypic defects, which include poor mating and delayed development; at the restrictive temperature, <em>apl-1</em>(yn5) mutants show an incompletely penetrant lethality. moa-1 mutations suppress the<em> apl-1</em>(yn5) lethality at the restrictive temperature. Surprisingly, <em>moa-1</em> is involved in male tail development; the male tail is critical for successful mating. This project focused on studying the morphology and mating behavior of yn5 mutants, <em>moa-1</em> transgenic animals, and other mutants regulating male tail development. Strains were characterized for morphology and mating behavior without knowledge of the genotype of the animals. Understanding male tail development may provide insights into other pathways in which <em>apl-1</em> functions.</p>"],"dc:identifier":["https://academicworks.cuny.edu/cc_etds_theses/780"],"dc:subject":["male tail morphogenesis nematode alzheimer's mating","Biology","Genetics and Genomics"],"dc:title":["Role of MOA-1, an Anti-phosphatase, and APL-1, an APP-related Protein, in Morphogenesis and Mating Behavior in Caenorhabditis elegans"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (M.S.)"]},"updated_at":"2026-07-24T01:57:21Z"}