The protein product of the JIL-1 gene is a tandem chromosomal kinase (referred to as JIL-1). Studies of JIL-1 P-element deletion and insertion loss-of-function mutations suggest that JIL-1 plays a role in histone H3 serine 10 phosphorylation, polytene chromosome morphology maintenance, dosage compensation pathways, and homeotic transformation pathways. Due to the limitation of deletion/insertion mutations, EMS mutagenesis was performed to induce point mutations of JIL-1 and the mutation screen was designed to recover temperature-sensitive JIL-1 alleles. 11 new mutant alleles were identified and 4 were selected for further analysis. The mutant phenotypes given by the four new JIL-1 alleles were characterized. Three of the four showed polytene chromosome phenotypes similar to those of individuals homozygous for a null allele of JIL-1, and one showed polytene chromosome phenotypes similar to those of individuals homozygous for a hypomorphic allele of JIL-1. All of the four mutations produce an adult male homeotic transformation phenotype similar to that of known JIL-1 hypomorphic alleles, even though the penetrance of this phenotype is not the same for each of the four mutations. Fluorescence-conjugated antibody staining of mutant chromosomes showed that for all four mutations the JIL-1 protein level was reduced and the localization of the JIL-1 staining was different from that of the wild type controls. Western blot analysis showed no detectable amounts of JIL-1 protein in mutant individuals for all four mutations. The DNA sequence of the JIL-1 gene of one of the new mutants, 29-1b, was determined and no significant base sequence changes were found in the open reading frame.
","abstract_html":"<p>The protein product of the JIL-1 gene is a tandem chromosomal kinase (referred to as JIL-1). Studies of JIL-1 P-element deletion and insertion loss-of-function mutations suggest that JIL-1 plays a role in histone H3 serine 10 phosphorylation, polytene chromosome morphology maintenance, dosage compensation pathways, and homeotic transformation pathways. Due to the limitation of deletion/insertion mutations, EMS mutagenesis was performed to induce point mutations of JIL-1 and the mutation screen was designed to recover temperature-sensitive JIL-1 alleles. 11 new mutant alleles were identified and 4 were selected for further analysis. The mutant phenotypes given by the four new JIL-1 alleles were characterized. Three of the four showed polytene chromosome phenotypes similar to those of individuals homozygous for a null allele of JIL-1, and one showed polytene chromosome phenotypes similar to those of individuals homozygous for a hypomorphic allele of JIL-1. All of the four mutations produce an adult male homeotic transformation phenotype similar to that of known JIL-1 hypomorphic alleles, even though the penetrance of this phenotype is not the same for each of the four mutations. Fluorescence-conjugated antibody staining of mutant chromosomes showed that for all four mutations the JIL-1 protein level was reduced and the localization of the JIL-1 staining was different from that of the wild type controls. Western blot analysis showed no detectable amounts of JIL-1 protein in mutant individuals for all four mutations. The DNA sequence of the JIL-1 gene of one of the new mutants, 29-1b, was determined and no significant base sequence changes were found in the open reading frame.</p>","abstract_has_math":false,"creators":["Huang, Shao-Yi"],"institution":null,"degree_name":"Master of Science","degree_level":"thesis","degree_discipline":"Genetics","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2005,"date_issued":"2005-01-01","date_published":"2005-01-01","updated_at":"2026-07-24T02:39:19Z","subjects":[],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["archive/lib.dr.iastate.edu/rtd/18798/"],"render_values":[{"text":"archive/lib.dr.iastate.edu/rtd/18798/","href":null,"code":true}]}]},"links":{"outbound_url":"https://dr.lib.iastate.edu/handle/20.500.12876/72736","outbound_label":"Repository record","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Huang, Shao-Yi"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-03-12T09:59:04.000"]},{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2020-06-30T08:10:39Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2020-06-30T08:10:39Z"]},{"key":"dc:date.issued","label":"Date","values":["2005-01-01"]},{"key":"dc:type","label":"Dc Type","values":["thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Genetics"]},{"key":"thesis:degree_level","label":"Degree Level","values":["thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["archive/lib.dr.iastate.edu/rtd/18798/"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://dr.lib.iastate.edu/handle/20.500.12876/72736"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The protein product of the JIL-1 gene is a tandem chromosomal kinase (referred to as JIL-1). Studies of JIL-1 P-element deletion and insertion loss-of-function mutations suggest that JIL-1 plays a role in histone H3 serine 10 phosphorylation, polytene chromosome morphology maintenance, dosage compensation pathways, and homeotic transformation pathways. Due to the limitation of deletion/insertion mutations, EMS mutagenesis was performed to induce point mutations of JIL-1 and the mutation screen was designed to recover temperature-sensitive JIL-1 alleles. 11 new mutant alleles were identified and 4 were selected for further analysis. The mutant phenotypes given by the four new JIL-1 alleles were characterized. Three of the four showed polytene chromosome phenotypes similar to those of individuals homozygous for a null allele of JIL-1, and one showed polytene chromosome phenotypes similar to those of individuals homozygous for a hypomorphic allele of JIL-1. All of the four mutations produce an adult male homeotic transformation phenotype similar to that of known JIL-1 hypomorphic alleles, even though the penetrance of this phenotype is not the same for each of the four mutations. Fluorescence-conjugated antibody staining of mutant chromosomes showed that for all four mutations the JIL-1 protein level was reduced and the localization of the JIL-1 staining was different from that of the wild type controls. Western blot analysis showed no detectable amounts of JIL-1 protein in mutant individuals for all four mutations. The DNA sequence of the JIL-1 gene of one of the new mutants, 29-1b, was determined and no significant base sequence changes were found in the open reading frame.
"]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Mutational analysis of JIL-1, a tandem kinase in Drosophila"]}]}],"canonical_facts":{"dc:creator":["Huang, Shao-Yi"],"dc:date":["2019-03-12T09:59:04.000"],"dc:date.accessioned":["2020-06-30T08:10:39Z"],"dc:date.available":["2020-06-30T08:10:39Z"],"dc:date.issued":["2005-01-01"],"dc:description.abstract":["The protein product of the JIL-1 gene is a tandem chromosomal kinase (referred to as JIL-1). Studies of JIL-1 P-element deletion and insertion loss-of-function mutations suggest that JIL-1 plays a role in histone H3 serine 10 phosphorylation, polytene chromosome morphology maintenance, dosage compensation pathways, and homeotic transformation pathways. Due to the limitation of deletion/insertion mutations, EMS mutagenesis was performed to induce point mutations of JIL-1 and the mutation screen was designed to recover temperature-sensitive JIL-1 alleles. 11 new mutant alleles were identified and 4 were selected for further analysis. The mutant phenotypes given by the four new JIL-1 alleles were characterized. Three of the four showed polytene chromosome phenotypes similar to those of individuals homozygous for a null allele of JIL-1, and one showed polytene chromosome phenotypes similar to those of individuals homozygous for a hypomorphic allele of JIL-1. All of the four mutations produce an adult male homeotic transformation phenotype similar to that of known JIL-1 hypomorphic alleles, even though the penetrance of this phenotype is not the same for each of the four mutations. Fluorescence-conjugated antibody staining of mutant chromosomes showed that for all four mutations the JIL-1 protein level was reduced and the localization of the JIL-1 staining was different from that of the wild type controls. Western blot analysis showed no detectable amounts of JIL-1 protein in mutant individuals for all four mutations. The DNA sequence of the JIL-1 gene of one of the new mutants, 29-1b, was determined and no significant base sequence changes were found in the open reading frame.
"],"dc:format.mimetype":["application/pdf"],"dc:identifier":["archive/lib.dr.iastate.edu/rtd/18798/"],"dc:identifier.uri":["https://dr.lib.iastate.edu/handle/20.500.12876/72736"],"dc:language.iso":["en"],"dc:title":["Mutational analysis of JIL-1, a tandem kinase in Drosophila"],"dc:type":["thesis"],"thesis:degree_discipline":["Genetics"],"thesis:degree_level":["thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T02:39:19Z"}