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Centrosome-intrinsic mechanisms modulate centrosome integrity during fever
#MMPMID26269579
Vertii A
; Zimmerman W
; Ivshina M
; Doxsey S
Mol Biol Cell
2015[Oct]; 26
(19
): 3451-63
PMID26269579
show ga
The centrosome is critical for cell division, ciliogenesis, membrane trafficking,
and immunological synapse function. The immunological synapse is part of the
immune response, which is often accompanied by fever/heat stress (HS). Here we
provide evidence that HS causes deconstruction of all centrosome substructures
primarily through degradation by centrosome-associated proteasomes. This renders
the centrosome nonfunctional. Heat-activated degradation is centrosome selective,
as other nonmembranous organelles (midbody, kinetochore) and membrane-bounded
organelles (mitochondria) remain largely intact. Heat-induced centrosome
inactivation was rescued by targeting Hsp70 to the centrosome. In contrast, Hsp70
excluded from the centrosome via targeting to membranes failed to rescue, as did
chaperone inactivation. This indicates that there is a balance between
degradation and chaperone rescue at the centrosome after HS. This novel mechanism
of centrosome regulation during fever contributes to immunological synapse
formation. Heat-induced centrosome inactivation is a physiologically relevant
event, as centrosomes in leukocytes of febrile patients are disrupted.
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