{"id":{"repo_id":"unr","oai_identifier":"oai:scholarwolf.unr.edu:11714/2500"},"canonical_url":"https://search.dev.ndltd.org/etd/unr/oai:scholarwolf.unr.edu:11714/2500","repository":{"repo_id":"unr","name":"University of Nevada - Reno","base_url":"https://scholarwolf.unr.edu/server/oai/request"},"display":{"title":"Defects in protein trafficking affect expression of GPCRs in C. elegans","abstract":"In the nematode C. elegans, the bilaterally symmetric PVQ neurons are located in the tail and each extends an axon along the ventral nerve cord to the head. Several G protein coupled receptors (EGL-47, SRA-6) are terminally expressed in PVQ as well as a limited number of other neurons. Mutations in six genes (tba-1, unc-14, unc-33, unc-44, unc-51, unc-119) known to disrupt axon outgrowth were found to eliminate expression of sra-6::gfp and egl-47::gfp in PVQ soon after hatching. Expression of sra-6::gfp was high in embryos and newly hatched L1 larvae, yet the GFP signal was greatly reduced within 2-3 hours and was typically not detectable after 10 hours. Expression of sra-6::gfp in the chemosensory neurons, ASH and ASI, was not affected. Previous studies reported that UNC-119 is an acylated protein transporter, and is required for transporting G protein α-subunits and other acylated proteins. However, loss of function of unc-119 does not affect the expression of G protein. Together, these results suggest that protein trafficking defects resulting from the loss of UNC-119 in turn lead to a reduction in gene transcription of sra-6 and egl-47. To understand further how these six genes affect transcription, we undertook a genetic screen to isolate mutations that restore expression of sra-6::gfp in PVQ in unc-119 mutants. Eight suppressors that define two genes were isolated. Unc-119 animals harboring a suppresser mutation still exhibit a strong Dpy and Unc unc-119 phenotype and PVQ still has axon outgrowth defects. As such, these suppressors are specific to the restoration of sra-6::gfp expression in PVQ and do not appear to rescue other unc-119 functions. The suppressors are also specific to unc-119 and do not restore expression of sra-6 in the other mutants.","abstract_html":"In the nematode C. elegans, the bilaterally symmetric PVQ neurons are located in the tail and each extends an axon along the ventral nerve cord to the head. Several G protein coupled receptors (EGL-47, SRA-6) are terminally expressed in PVQ as well as a limited number of other neurons. Mutations in six genes (tba-1, unc-14, unc-33, unc-44, unc-51, unc-119) known to disrupt axon outgrowth were found to eliminate expression of sra-6::gfp and egl-47::gfp in PVQ soon after hatching. Expression of sra-6::gfp was high in embryos and newly hatched L1 larvae, yet the GFP signal was greatly reduced within 2-3 hours and was typically not detectable after 10 hours. Expression of sra-6::gfp in the chemosensory neurons, ASH and ASI, was not affected. Previous studies reported that UNC-119 is an acylated protein transporter, and is required for transporting G protein α-subunits and other acylated proteins. However, loss of function of unc-119 does not affect the expression of G protein. Together, these results suggest that protein trafficking defects resulting from the loss of UNC-119 in turn lead to a reduction in gene transcription of sra-6 and egl-47. To understand further how these six genes affect transcription, we undertook a genetic screen to isolate mutations that restore expression of sra-6::gfp in PVQ in unc-119 mutants. Eight suppressors that define two genes were isolated. Unc-119 animals harboring a suppresser mutation still exhibit a strong Dpy and Unc unc-119 phenotype and PVQ still has axon outgrowth defects. As such, these suppressors are specific to the restoration of sra-6::gfp expression in PVQ and do not appear to rescue other unc-119 functions. The suppressors are also specific to unc-119 and do not restore expression of sra-6 in the other mutants.","abstract_has_math":false,"creators":["Gorzalski, Andrew J."],"institution":null,"degree_name":null,"degree_level":"Doctorate Degree","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Clark, Scott G."],"committee_chairs":[],"committee_members":["Kidd, Thomas","Berninsone, Patricia","Keene, Alex","Miller, Glenn"],"year":2015,"date_issued":"2015","date_published":"2015","updated_at":"2026-07-27T21:46:41Z","subjects":["C. elegans","gene expression","GPCR","Trafficking"],"languages":[],"rights":["In Copyright(All Rights Reserved)"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/11714/2500","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Clark, Scott G."]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Kidd, Thomas","Berninsone, Patricia","Keene, Alex","Miller, Glenn"]},{"key":"dc:creator","label":"Author","values":["Gorzalski, Andrew J."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2018-01-08T17:36:47Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2018-01-08T17:36:47Z"]},{"key":"dc:date.issued","label":"Date","values":["2015"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Doctorate Degree"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["C. elegans","gene expression","GPCR","Trafficking"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["In Copyright(All Rights Reserved)"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/11714/2500"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["In the nematode C. elegans, the bilaterally symmetric PVQ neurons are located in the tail and each extends an axon along the ventral nerve cord to the head. Several G protein coupled receptors (EGL-47, SRA-6) are terminally expressed in PVQ as well as a limited number of other neurons. Mutations in six genes (tba-1, unc-14, unc-33, unc-44, unc-51, unc-119) known to disrupt axon outgrowth were found to eliminate expression of sra-6::gfp and egl-47::gfp in PVQ soon after hatching. Expression of sra-6::gfp was high in embryos and newly hatched L1 larvae, yet the GFP signal was greatly reduced within 2-3 hours and was typically not detectable after 10 hours. Expression of sra-6::gfp in the chemosensory neurons, ASH and ASI, was not affected. Previous studies reported that UNC-119 is an acylated protein transporter, and is required for transporting G protein α-subunits and other acylated proteins. However, loss of function of unc-119 does not affect the expression of G protein. Together, these results suggest that protein trafficking defects resulting from the loss of UNC-119 in turn lead to a reduction in gene transcription of sra-6 and egl-47. To understand further how these six genes affect transcription, we undertook a genetic screen to isolate mutations that restore expression of sra-6::gfp in PVQ in unc-119 mutants. Eight suppressors that define two genes were isolated. Unc-119 animals harboring a suppresser mutation still exhibit a strong Dpy and Unc unc-119 phenotype and PVQ still has axon outgrowth defects. As such, these suppressors are specific to the restoration of sra-6::gfp expression in PVQ and do not appear to rescue other unc-119 functions. The suppressors are also specific to unc-119 and do not restore expression of sra-6 in the other mutants."]},{"key":"dc:format","label":"Dc Format","values":["PDF"]},{"key":"dc:title","label":"Title","values":["Defects in protein trafficking affect expression of GPCRs in C. elegans"]}]}],"canonical_facts":{"dc:contributor.advisor":["Clark, Scott G."],"dc:contributor.committeemember":["Kidd, Thomas","Berninsone, Patricia","Keene, Alex","Miller, Glenn"],"dc:creator":["Gorzalski, Andrew J."],"dc:date.accessioned":["2018-01-08T17:36:47Z"],"dc:date.available":["2018-01-08T17:36:47Z"],"dc:date.issued":["2015"],"dc:description.abstract":["In the nematode C. elegans, the bilaterally symmetric PVQ neurons are located in the tail and each extends an axon along the ventral nerve cord to the head. Several G protein coupled receptors (EGL-47, SRA-6) are terminally expressed in PVQ as well as a limited number of other neurons. Mutations in six genes (tba-1, unc-14, unc-33, unc-44, unc-51, unc-119) known to disrupt axon outgrowth were found to eliminate expression of sra-6::gfp and egl-47::gfp in PVQ soon after hatching. Expression of sra-6::gfp was high in embryos and newly hatched L1 larvae, yet the GFP signal was greatly reduced within 2-3 hours and was typically not detectable after 10 hours. Expression of sra-6::gfp in the chemosensory neurons, ASH and ASI, was not affected. Previous studies reported that UNC-119 is an acylated protein transporter, and is required for transporting G protein α-subunits and other acylated proteins. However, loss of function of unc-119 does not affect the expression of G protein. Together, these results suggest that protein trafficking defects resulting from the loss of UNC-119 in turn lead to a reduction in gene transcription of sra-6 and egl-47. To understand further how these six genes affect transcription, we undertook a genetic screen to isolate mutations that restore expression of sra-6::gfp in PVQ in unc-119 mutants. Eight suppressors that define two genes were isolated. Unc-119 animals harboring a suppresser mutation still exhibit a strong Dpy and Unc unc-119 phenotype and PVQ still has axon outgrowth defects. As such, these suppressors are specific to the restoration of sra-6::gfp expression in PVQ and do not appear to rescue other unc-119 functions. The suppressors are also specific to unc-119 and do not restore expression of sra-6 in the other mutants."],"dc:format":["PDF"],"dc:identifier.uri":["http://hdl.handle.net/11714/2500"],"dc:rights":["In Copyright(All Rights Reserved)"],"dc:subject":["C. elegans","gene expression","GPCR","Trafficking"],"dc:title":["Defects in protein trafficking affect expression of GPCRs in C. elegans"],"dc:type":["Dissertation"],"thesis:degree_level":["Doctorate Degree"]},"updated_at":"2026-07-27T21:46:41Z"}