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SUMMARY:Cell cycle controls enforcing asymmetric spindle pole fate in budd
 ing yeast - Dr Marisa Segal from Department of Genetics\, University of Ca
 mbridge 
DTSTART:20181122T140000Z
DTEND:20181122T150000Z
UID:TALK109234@talks.cam.ac.uk
CONTACT:Caroline Newnham
DESCRIPTION:A multicellular organism consists of a variety of cell types s
 haring the same original genetic instructions. This diversity arises partl
 y from asymmetric cell divisions in which the two daughter progeny cells a
 dopt different fates. In particular\, stem cells may divide symmetrically 
 to expand their pool\, but it is through self-renewing asymmetric cell div
 isions that they generate two progeny cells with distinct identities in a 
 balanced manner. One will commit to differentiate while the other will ret
 ain its stem cell potential for unlimited proliferation. The loss of this 
 balance may lead to cancer.\n\nWe study asymmetric cell division in the bu
 dding yeast S. cerevisiae. In yeast\, pole-derived astral microtubules (aM
 Ts) position the spindle to intersect the bud neck\, a configuration contr
 olled by the spindle pole body (SPB\, the counterpart of the centrosome). 
 Initially\, the "old" SPB (from the preceding cell cycle) reaches for the 
 bud via its existing aMTs\, while the newly duplicated SPB acquires aMTs l
 ater. The asymmetric presence of aMTs commits the old SPB to the bud withi
 n a window of opportunity\, thus promoting an invariant age-dependent patt
 ern of SPB inheritance. Self-renewing stem cell divisions showcase similar
  stereotyped patterns of centrosome inheritance.\n\nWe have uncovered a st
 ructural asymmetry involving the site for aMT organisation - the SPB outer
  plaque. Indeed\, recruitment of the gamma-tubulin nucleation complex favo
 urs the old SPB\, a bias dictated by the initial absence of its receptor S
 pc72 at the new SPB outer plaque. These findings suggest that the new SPB 
 is incompletely built by the time of SPB separation\, to enforce asymmetry
 \, with Spc72 representing the most upstream factor linking SPB history an
 d fate. Here\, I will discuss our current understanding of SPB dynamic ass
 embly and the mechanisms linking cell cycle control with SPB functional as
 ymmetry.\n
LOCATION:Biffen Lecture Theatre\, Department of Genetics\, Downing Site
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