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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Curr+Biol
2014 ; 24
(19
): 2327-2334
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A unique set of centrosome proteins requires pericentrin for spindle-pole
localization and spindle orientation
#MMPMID25220058
Chen CT
; Hehnly H
; Yu Q
; Farkas D
; Zheng G
; Redick SD
; Hung HF
; Samtani R
; Jurczyk A
; Akbarian S
; Wise C
; Jackson A
; Bober M
; Guo Y
; Lo C
; Doxsey S
Curr Biol
2014[Oct]; 24
(19
): 2327-2334
PMID25220058
show ga
Majewski osteodysplastic primordial dwarfism type II (MOPDII) is caused by
mutations in the centrosome gene pericentrin (PCNT) that lead to severe pre- and
postnatal growth retardation. As in MOPDII patients, disruption of pericentrin
(Pcnt) in mice caused a number of abnormalities including microcephaly, aberrant
hemodynamics analyzed by in utero echocardiography, and cardiovascular anomalies;
the latter being associated with mortality, as in the human condition. To
identify the mechanisms underlying these defects, we tested for changes in cell
and molecular function. All Pcnt(-/-) mouse tissues and cells examined showed
spindle misorientation. This mouse phenotype was associated with misdirected
ventricular septal growth in the heart, decreased proliferative symmetric
divisions in brain neural progenitors, and increased misoriented divisions in
fibroblasts; the same phenotype was seen in fibroblasts from three MOPDII
individuals. Misoriented spindles were associated with disrupted astral
microtubules and near complete loss of a unique set of centrosome proteins from
spindle poles (ninein, Cep215, centriolin). All these proteins appear to be
crucial for microtubule anchoring and all interacted with Pcnt, suggesting that
Pcnt serves as a molecular scaffold for this functionally linked set of spindle
pole proteins. Importantly, Pcnt disruption had no detectable effect on
localization of proteins involved in the cortical polarity pathway (NuMA,
p150(glued), aPKC). Not only do these data reveal a spindle-pole-localized
complex for spindle orientation, but they identify key spindle symmetry proteins
involved in the pathogenesis of MOPDII.
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