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Departmental seminar - Marisa Segal : Cell Cycle Controls Enforcing Asymmetric Spindle Pole Fate in Budding Yeast

When Nov 22, 2018
from 02:00 PM to 03:00 PM
Where Biffen Lecture Theatre, underneath Dept of Genetics
Contact Name Helene Rangone-Briatte
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The Genetics Seminar Series talk will be at 14:00 in the Biffen Lecture Theatre on Thursday 22nd November 2018.  There will also be an opportunity to meet the speaker in the Department of Genetics tea room immediately after the talk from 15:00 until 15:30 and biscuits will be provided. 

Dr Marisa Segal from Department of Genetics, University of Cambridge will be speaking and the title of the talk is,

''Cell cycle controls enforcing asymmetric spindle pole fate in budding yeast''

A multicellular organism consists of a variety of cell types sharing the same original genetic instructions. This diversity arises partly from asymmetric cell divisions in which the two daughter progeny cells adopt different fates. In particular, stem cells may divide symmetrically to expand their pool, but it is through self-renewing asymmetric cell divisions that they generate two progeny cells with distinct identities in a balanced manner. One will commit to differentiate while the other will retain its stem cell potential for unlimited proliferation. The loss of this balance may lead to cancer.

We study asymmetric cell division in the budding yeast S. cerevisiae. In yeast, pole-derived astral microtubules (aMTs) position the spindle to intersect the bud neck, a configuration controlled 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 later. The asymmetric presence of aMTs commits the old SPB to the bud within a window of opportunity, thus promoting an invariant age-dependent pattern of SPB inheritance. Self-renewing stem cell divisions showcase similar stereotyped patterns of centrosome inheritance.

We have uncovered a structural asymmetry involving the site for aMT organisation - the SPB outer plaque. Indeed, recruitment of the gamma-tubulin nucleation complex favours the old SPB, a bias dictated by the initial absence of its receptor Spc72 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 and fate. Here, I will discuss our current understanding of SPB dynamic assembly and the mechanisms linking cell cycle control with SPB functional asymmetry.

Host: Helene Rangone-Briatte