The telomere bouquet is a highly conserved structure specific to meiotic prophase
in which the telomeres are gathered to a limited region of the nuclear periphery.
In a number of organisms including fission yeast, the bouquet is tethered to the
spindle pole body (SPB) or centrosome. The meiosis-specific factors Bqt1/Bqt2
function as a bridge to connect the telomere proteins Taz1/Rap1 to the SPB.
Deletion of any of these elements disrupts the bouquet, leading to defective
spindle formation and aberrant meiosis (Tomita and Cooper, 2007). The aim of
this thesis was to determine the molecular basis for control of the meiotic spindle
by the telomere bouquet. We asked the question: how does the meiotic SPB differ
in the presence and absence of bouquet function? Using methods to quantify SPB
component levels via fluorescence microscopy in live cells, we found that
bouquet-defective strains show a slight elevation of the level of Pcp1, an SPB
component, but such elevation is not enough to confer bouquet-mutant
phenotypes in bouquet-proficient backgrounds. Indeed, our data suggest that in
the absence of the bouquet, SPB duplication occurs properly and with normal
timing. However, we observed that the separation of the duplicated SPBs is
markedly abnormal, as the duplicated SPBs fail to remain apart and at least one of
them often becomes dislodged from the nucleus. Moreover, the γ-tubulin complex
fails to localise to both spindle poles. Hence, the duplicated SPBs fail to properly
recruit the γ-tubulin complex. We thus investigated the molecular mechanism
underlying control of γ-tubulin complex recruitment by the bouquet. Our findings
allow us to propose a model that explains the different types of spindle defects
seen in the absence of the bouquet
