From a genetic and allelic modifier screen, we report that the Drosophila melanogaster T-box transcription factor midline (mid), a homolog to the human TBX20 gene, interacts with dFOXO within the insulin receptor (InR) and the c-Jun-N-terminal kinase (JNK) signaling pathways to regulate interommatidial bristle (IOB) formation. Previous studies have identified mid’s role in cell fate specification of sensory organ precursor cells in conjunction with the Notch-Delta signaling pathway (Das et al., 2013). The Notch, InR, and JNK signaling pathways regulate dFOXO activity under conditions of stress. Thus, we determined the effects of oxidative stress and metabolic stress by exposing mid-RNAi flies to paraquat and starvation conditions, respectively. We found that oxidative stress suppressed the mid-RNAi phenotype while starvation had no significant effect. We next assayed Mid and H15, a paralog of Mid, via Western blot analysis and report that Mid exhibits a nucleocytoplasmic distribution pattern that is altered within the mid-RNAi mutant while H15 was found exclusively within the cytoplasmic fraction. This opens the possibility that Mid and/or H15 may regulate cytoplasmic targets upstream of dFOXO. The evidence suggests that Mid utilizes the InR, JNK, and Notch signaling pathways to regulate cell fate specification, differentiation, and survival during third instar larval development.
","abstract_html":"<p>From a genetic and allelic modifier screen, we report that the <em>Drosophila melanogaster </em>T-box transcription factor <em>midline (mid)</em>, a homolog to the human <em>TBX20 </em>gene, interacts with <em>dFOXO </em>within the insulin receptor (InR) and the c-Jun-N-terminal kinase (JNK) signaling pathways to regulate interommatidial bristle (IOB) formation. Previous studies have identified <em>mid</em>’s role in cell fate specification of sensory organ precursor cells in conjunction with the Notch-Delta signaling pathway (Das et al., 2013). The Notch, InR, and JNK signaling pathways regulate dFOXO activity under conditions of stress. Thus, we determined the effects of oxidative stress and metabolic stress by exposing <em>mid</em>-RNAi flies to paraquat and starvation conditions, respectively. We found that oxidative stress suppressed the <em>mid</em>-RNAi phenotype while starvation had no significant effect. We next assayed Mid and H15, a paralog of Mid, via Western blot analysis and report that Mid exhibits a nucleocytoplasmic distribution pattern that is altered within the <em>mid</em>-RNAi mutant while H15 was found exclusively within the cytoplasmic fraction. This opens the possibility that Mid and/or H15 may regulate cytoplasmic targets upstream of dFOXO. The evidence suggests that Mid utilizes the InR, JNK, and Notch signaling pathways to regulate cell fate specification, differentiation, and survival during third instar larval development.</p>","abstract_has_math":false,"creators":["Chen, Qichuan"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Masters Thesis","degree_discipline":"Biological Sciences","degree_department":null,"school":null,"contributors":["Sandra Leal","Hao Xu","Janis O'Donnell"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-12-01T08:00:00Z","date_published":"2014-12-01T08:00:00Z","updated_at":"2026-07-24T05:44:27Z","subjects":["mid","midline","Tbx20","dFOXO","C-Jun-N-terminal kinase","insulin receptor","Developmental Biology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://aquila.usm.edu/masters_theses/76","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Sandra Leal","Hao Xu","Janis O'Donnell"]},{"key":"dc:creator","label":"Author","values":["Chen, Qichuan"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2014-07-01T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biological Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["mid","midline","Tbx20","dFOXO","C-Jun-N-terminal kinase","insulin receptor","Developmental Biology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://aquila.usm.edu/masters_theses/76"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["From a genetic and allelic modifier screen, we report that the Drosophila melanogaster T-box transcription factor midline (mid), a homolog to the human TBX20 gene, interacts with dFOXO within the insulin receptor (InR) and the c-Jun-N-terminal kinase (JNK) signaling pathways to regulate interommatidial bristle (IOB) formation. Previous studies have identified mid’s role in cell fate specification of sensory organ precursor cells in conjunction with the Notch-Delta signaling pathway (Das et al., 2013). The Notch, InR, and JNK signaling pathways regulate dFOXO activity under conditions of stress. Thus, we determined the effects of oxidative stress and metabolic stress by exposing mid-RNAi flies to paraquat and starvation conditions, respectively. We found that oxidative stress suppressed the mid-RNAi phenotype while starvation had no significant effect. We next assayed Mid and H15, a paralog of Mid, via Western blot analysis and report that Mid exhibits a nucleocytoplasmic distribution pattern that is altered within the mid-RNAi mutant while H15 was found exclusively within the cytoplasmic fraction. This opens the possibility that Mid and/or H15 may regulate cytoplasmic targets upstream of dFOXO. The evidence suggests that Mid utilizes the InR, JNK, and Notch signaling pathways to regulate cell fate specification, differentiation, and survival during third instar larval development.
"]},{"key":"dc:title","label":"Title","values":["The Drosophila T-box Transcription Factor Midline Functions within the Insulin/AKT and c-Jun-N-terminal Kinase Signaling Pathways to Regulate Interomatidial Bristle Formation and Cell Survival"]}]}],"canonical_facts":{"dc:contributor":["Sandra Leal","Hao Xu","Janis O'Donnell"],"dc:creator":["Chen, Qichuan"],"dc:date.available":["2014-07-01T07:00:00Z"],"dc:description.abstract":["From a genetic and allelic modifier screen, we report that the Drosophila melanogaster T-box transcription factor midline (mid), a homolog to the human TBX20 gene, interacts with dFOXO within the insulin receptor (InR) and the c-Jun-N-terminal kinase (JNK) signaling pathways to regulate interommatidial bristle (IOB) formation. Previous studies have identified mid’s role in cell fate specification of sensory organ precursor cells in conjunction with the Notch-Delta signaling pathway (Das et al., 2013). The Notch, InR, and JNK signaling pathways regulate dFOXO activity under conditions of stress. Thus, we determined the effects of oxidative stress and metabolic stress by exposing mid-RNAi flies to paraquat and starvation conditions, respectively. We found that oxidative stress suppressed the mid-RNAi phenotype while starvation had no significant effect. We next assayed Mid and H15, a paralog of Mid, via Western blot analysis and report that Mid exhibits a nucleocytoplasmic distribution pattern that is altered within the mid-RNAi mutant while H15 was found exclusively within the cytoplasmic fraction. This opens the possibility that Mid and/or H15 may regulate cytoplasmic targets upstream of dFOXO. The evidence suggests that Mid utilizes the InR, JNK, and Notch signaling pathways to regulate cell fate specification, differentiation, and survival during third instar larval development.
"],"dc:identifier":["https://aquila.usm.edu/masters_theses/76"],"dc:subject":["mid","midline","Tbx20","dFOXO","C-Jun-N-terminal kinase","insulin receptor","Developmental Biology"],"dc:title":["The Drosophila T-box Transcription Factor Midline Functions within the Insulin/AKT and c-Jun-N-terminal Kinase Signaling Pathways to Regulate Interomatidial Bristle Formation and Cell Survival"],"thesis:degree_discipline":["Biological Sciences"],"thesis:degree_level":["Masters Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T05:44:27Z"}