Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760330
Title: Function of Kek-6 and DNT2 in structural synaptic plasticity in Drosophila
Author: Ulian Benitez, Suzana
ISNI:       0000 0004 7432 3208
Awarding Body: University of Birmingham
Current Institution: University of Birmingham
Date of Award: 2018
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Abstract:
The Drosophila nervous system undergoes structural synaptic plasticity, however, the mechanisms that govern such event are little understood. Structural synaptic plasticity in mammals is regulated by the neurotrophin brain derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase full length (TrkB-FL). TrkB-FL has a tyrosine kinase domain (TyrK) intracellularly, that is required for its function in structural synaptic plasticity. Trk receptors have long been sought in Drosophila to verify mechanisms of structural synaptic plasticity, but they have not been found. Later, the Kek receptor family was identified as the kinaseless-Trk homologues in flies (Mandai et al., 2009, Bishop, 2013). Here, I validated that Kek-6 is a neurotrophin receptor for DNT2. DNT2 is a novel retrograde factor at the neuromuscular junction (NMJ), and both DNT2 and Kek-6 regulate structural synaptic plasticity. Kek-6 functions in concert with Toll-6. DNT2 and Kek-6 function upstream of CaMKII and Vap33A at the NMJ synapse. Finally, I show that Kek-6 can regulate intracellular levels of calcium in larval motorneurons. In conclusion, I identified a novel mechanism of structural synaptic plasticity in flies that is independent of a TyrK domain. If there are conserved mechanisms, this may also shed light on how truncated Trks function in the adult mammalian brain.
Supervisor: Not available Sponsor: Science Without Borders
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.760330  DOI: Not available
Keywords: QH301 Biology ; RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
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