{"id":{"repo_id":"wustl","oai_identifier":"oai:openscholarship.wustl.edu:etd-1871"},"canonical_url":"https://search.dev.ndltd.org/etd/wustl/oai:openscholarship.wustl.edu:etd-1871","repository":{"repo_id":"wustl","name":"Washington University in St. Louis","base_url":"https://openscholarship.wustl.edu/do/oai/"},"display":{"title":"A DLK And JNK Dependent Axon Self-Destruction Program Promotes Wallerian Degeneration","abstract":"Axon loss is a debilitating consequence of a wide range of neurological conditions. As axons degenerate, they go through a stereotyped sequence of morphological changes termed Wallerian degeneration. It has long been hypothesized that there is an active axonal breakdown program, conceptually similar to apoptosis, which underlies Wallerian degeneration. However, the molecular pathways that accomplish this program in neurons have remained elusive. We demonstrate that dual leucine kinase: DLK) promotes degeneration of severed axons in Drosophila and mice, and its target JNK promotes degeneration locally in axons as they commit to degenerate. This pathway also promotes degeneration after chemotherapy exposure, and thus may be a component of a general axon self-destruction program.","abstract_html":"Axon loss is a debilitating consequence of a wide range of neurological conditions. As axons degenerate, they go through a stereotyped sequence of morphological changes termed Wallerian degeneration. It has long been hypothesized that there is an active axonal breakdown program, conceptually similar to apoptosis, which underlies Wallerian degeneration. However, the molecular pathways that accomplish this program in neurons have remained elusive. We demonstrate that dual leucine kinase: DLK) promotes degeneration of severed axons in Drosophila and mice, and its target JNK promotes degeneration locally in axons as they commit to degenerate. This pathway also promotes degeneration after chemotherapy exposure, and thus may be a component of a general axon self-destruction program.","abstract_has_math":false,"creators":["Miller, Bradley"],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Biology and Biomedical Sciences: Neurosciences","degree_department":null,"school":null,"contributors":["Aaron DiAntonio"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-24T07:00:00Z","date_published":"2011-05-24T07:00:00Z","updated_at":"2026-07-24T06:13:23Z","subjects":["Neurosciences","Axon Degeneration","DLK","JNK"],"languages":["English (en)"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.7936/K79K4889"],"render_values":[{"text":"https://doi.org/10.7936/K79K4889","href":"https://doi.org/10.7936/K79K4889","code":true}]}]},"links":{"outbound_url":"https://openscholarship.wustl.edu/etd/872","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Aaron DiAntonio"]},{"key":"dc:creator","label":"Author","values":["Miller, Bradley"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2013-05-25T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology and Biomedical Sciences: Neurosciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy (PhD)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Neurosciences","Axon Degeneration","DLK","JNK"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English (en)"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://openscholarship.wustl.edu/etd/872"]},{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.7936/K79K4889"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Axon loss is a debilitating consequence of a wide range of neurological conditions. As axons degenerate, they go through a stereotyped sequence of morphological changes termed Wallerian degeneration. It has long been hypothesized that there is an active axonal breakdown program, conceptually similar to apoptosis, which underlies Wallerian degeneration. However, the molecular pathways that accomplish this program in neurons have remained elusive. We demonstrate that dual leucine kinase: DLK) promotes degeneration of severed axons in Drosophila and mice, and its target JNK promotes degeneration locally in axons as they commit to degenerate. This pathway also promotes degeneration after chemotherapy exposure, and thus may be a component of a general axon self-destruction program."]},{"key":"dc:title","label":"Title","values":["A DLK And JNK Dependent Axon Self-Destruction Program Promotes Wallerian Degeneration"]}]}],"canonical_facts":{"dc:contributor":["Aaron DiAntonio"],"dc:creator":["Miller, Bradley"],"dc:date.available":["2013-05-25T07:00:00Z"],"dc:description.abstract":["Axon loss is a debilitating consequence of a wide range of neurological conditions. As axons degenerate, they go through a stereotyped sequence of morphological changes termed Wallerian degeneration. It has long been hypothesized that there is an active axonal breakdown program, conceptually similar to apoptosis, which underlies Wallerian degeneration. However, the molecular pathways that accomplish this program in neurons have remained elusive. We demonstrate that dual leucine kinase: DLK) promotes degeneration of severed axons in Drosophila and mice, and its target JNK promotes degeneration locally in axons as they commit to degenerate. This pathway also promotes degeneration after chemotherapy exposure, and thus may be a component of a general axon self-destruction program."],"dc:identifier":["https://openscholarship.wustl.edu/etd/872"],"dc:identifier.doi":["https://doi.org/10.7936/K79K4889"],"dc:language":["English (en)"],"dc:subject":["Neurosciences","Axon Degeneration","DLK","JNK"],"dc:title":["A DLK And JNK Dependent Axon Self-Destruction Program Promotes Wallerian Degeneration"],"thesis:degree_discipline":["Biology and Biomedical Sciences: Neurosciences"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T06:13:23Z"}