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UID:862@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20190902T130000

DTEND;TZID=Asia/Jerusalem:20190902T140000

DTSTAMP:20210802T125857Z

URL:https://biology.technion.ac.il/en/seminars/msc-graduate-seminar-yael-i
 osilevskii-2/

SUMMARY:MSC Graduate Seminar-Yael Iosilevskii [No Categories]
DESCRIPTION:Location:   \n Affiliation: \n Host:\n Research Topic:Functions
  for git-1in dendritic maintenance and behavior in Caenorhabditis elegansT
 he protein GIT1 (G-protein-coupled receptorkinase interacting ArfGAP 1) is
  a GTPase activating protein (GAP) for the Arfsmall GTP-binding proteins\,
  and a focal-adhesion-based scaffold\, with over 100associated proteins. G
 IT1 has been linked to dendritic spine formation andsynaptic changes in ro
 dent hippocampus\, as well as impairment in fear responseand learning. It 
 has also been implicated in Huntington’s disease\,Schizophrenia\, and AD
 HD (reviewed in 1). Inorder to study the effects of GIT1 on dendritic morp
 hology\, we use C.elegansand its stereotypically-arborized polymodal neuro
 n PVD (2) and follow its dendritic arborizationpattern and associated beha
 vioral outputs. We found that while git-1mutantsdisplay relatively normal 
 PVD neuron morphology in L4 stage\, this is followedby a significant and a
 symmetric increase in tertiary and quaternary ectopicbranches during early
  adulthood. Thus\, git-1 isnecessary for dendritic maintenance\, but not m
 orphogenesis. To reveal thesignaling pathway mediating this effect\, we te
 sted mutants of the GIT-1 primarybinding partner PIX (p21-activated kinase
  [PAK]-interacting exchange factor)and its downstream kinase PAK. We found
  that pix-1mutants have a similar\, yet milder\, phenotype in adult PVD mo
 rphology\, but pak-1 andhomologue max-2 mutants are wild-type-like\, sugge
 stingthat git-1 acts partly through its binding partner pix-1 as anegative
  regulator of branch arborization in adulthood. The behavioralphenotypes a
 ssociated with git-1 weretested by movement analysis and a harsh touch res
 ponse assay\, where we showthat two git-1 mutant alleles have no apparentm
 echanosensory defects but display increased speed and body wavelength. The
 seresults open a possibility for a novel dendritic maintenance pathway\, w
 hich mayinfluence proprioceptive faculties in the worm.  

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DTSTART:20190329T030000

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