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Title page for ETD etd-082809-160325


Document Typethesis
Author NamePlada, Edith Vanina Machado
URNetd-082809-160325
TitleAnalysis of the Kekkon Family in Neuronal Development
DegreeMS
DepartmentBiology & Biotechnology
Advisors
  • Joseph Duffy, Advisor
  • Elizabeth Ryder, Committee Member
  • Reeta Prusty Rao, Committee Member
  • Keywords
  • Kekkon
  • LIG
  • Development
  • GAL4
  • RNAi
  • nervous system
  • Drosophila
  • Date of Presentation/Defense2009-08-12
    Availability restricted

    Abstract

    Adhesion Molecules have been associated with a number of

    neurological and psychological disorders (humans), and

    implicated in various developmental processes (animals). Better

    understanding the development of the nervous system and the

    roles of adhesion molecules in it may be crucial to better

    understanding these disorders. LIGs, Leucine Rich Repeat and

    ImmunoGlobulin containing transmembrane proteins, represent

    a novel class of such adhesion molecules and have been

    implicated in various neuronal processes, including neurite

    outgrowth, axonal pathfinding, neuronal regeneration and

    survival. Two such LIGs are Kek1 and Kek2, members of a

    Drosophila LIG family, which have been reported to function in

    axonal pathfinding and synaptic plasticity, respectively. It is

    unclear what their roles in these processes are, as well as if

    other members of the Drosophila LIG family have similar roles.

    Current studies aim to survey the Kekkon family function in the

    nervous system, looking to identify new phenotypes and/or to

    elucidate the mechanisms underlying previously identified

    phenotypes.

    To achieve this goal, tissue specific inducible RNAi technique

    was employed. Validating of a number of transgenic RNAi stocks

    obtained was necessary and showed that all stocks obtained

    promoted specific and efficient knock down of target gene. Next

    an assessment of RNAi knockdown efficacy in developing

    nervous system was carried out and knockdown was shown to

    be weak if not in the presence of Dicer-2 co-misexpression. A

    number of screens for general behavioral phenotypes were

    performed including ubiquitous, neural, and imaginal discs

    knockdown. These uncovered possible effects of kek1 neural

    knockdown, as well as possible interaction of Kek1 with

    neurotactin, neuroglian and kek2. NMJ analysis of Kek5 and

    Kek6 was also carried out and preliminary results indicate

    possible interaction of kek5 in NMJ, although no statistical

    significance was detected.

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