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SUMMARY:The Elongator complex controls symmetry breaking of the central sp
 indle and thereby polarized trafficking of cell fate determinants during a
 symmetric cell division  - Vicente Jose Planelles Herrero – Derivery gro
 up – MRC LMB
DTSTART:20200226T173000Z
DTEND:20200226T193000Z
UID:TALK139819@talks.cam.ac.uk
CONTACT:Alexis
DESCRIPTION:Asymmetric cell division gives rise to two daughter cells that
  inherit different determinants\, thereby acquiring different fates. The p
 olarized sorting of signalling endosomes from an asymmetric central spindl
 e has emerged as an important feature of asymmetric cell division in Droso
 phila Sensory Organ Precursors (SOP). However\, how symmetry breaking of t
 he central spindle occurs in vivo remains poorly understood. Here\, we hav
 e identified the Elongator complex as a new player in this pathway. Elonga
 tor is a multiprotein complex involved in the regulation of transcription 
 and translation through histone acetylation and tRNA methylation\, respect
 ively. We found that\, in SOPs\, Elongator localizes to the central spindl
 e\, and that deletion of the catalytical subunit Elp3 abolishes central sp
 indle asymmetry and\, accordingly\, Sara endosome asymmetric segregation. 
 As Sara endosomes contain the cell fate determinants Notch and Delta\, thi
 s induces cell fate phenotypes in the adult fly. We further investigated t
 he molecular mechanism by which Elongator breaks the symmetry of the centr
 al spindle. Mammalian Elongator has previously been proposed to acetylate 
 microtubules\, potentially controlling their dynamics. However\, we found 
 that Drosophila Elongator does not acetylate tubulin and that Elp3 mutants
  can be rescued with an acetylase-dead version of Elp3 in vivo. Rather\, w
 e found that Elongator binds to microtubules\, lowering their frequency of
  catastrophe in in vitro single molecule assays\, suggesting that Elongato
 r asymmetrically stabilizes microtubules on one side of the central spindl
 e\, thereby generating central spindle asymmetry. We demonstrate this by m
 odifying the Elongator activity gradient through asymmetric targeting of E
 longator to the anterior cortex\, perturbing Sara endosome asymmetric segr
 egation. Altogether\, our data suggests that Elongator constitutes a novel
  link between polarity cues at the cell cortex and symmetry breaking of th
 e microtubule cytoskeleton.
LOCATION:Gurdon Institute Tea Room
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