scholarly journals WD40-repeat protein 62 is a JNK-phosphorylated spindle pole protein required for spindle maintenance and timely mitotic progression

2012 ◽  
Vol 125 (21) ◽  
pp. 5096-5109 ◽  
Author(s):  
M. A. Bogoyevitch ◽  
Y. Y. C. Yeap ◽  
Z. Qu ◽  
K. R. Ngoei ◽  
Y. Y. Yip ◽  
...  
2008 ◽  
Vol 17 (4) ◽  
pp. 163-170 ◽  
Author(s):  
Myung Whan Suh ◽  
Dong Hoon Shin ◽  
Ho Sun Lee ◽  
Ji Yeong Park ◽  
Chong Sun Kim ◽  
...  

Unlike mammals, avian cochlear hair cells can regenerate after acoustic overstimulation. The WDR1 gene is one of the genes suspected to play an important role in this difference. In an earlier study, we found that the WDR1 gene is over-expressed in the chick cochlea after acoustic overstimulation. The aim of this study was to compare the expression of WDR1 before and after acoustic overstimulation in the chick vestibule. Seven-day-old chicks were divided into three groups: normal group, damage group, and regeneration group. The damage and regeneration group was exposed to 120 dB SPL white noise for 5–6 hours. The damage group was euthanized shortly after the impulse, but the regeneration group was allowed to recover for 2 days. The utricle, saccule, and the three ampullae of each semicircular canal were dissected and immunohistochemically stained with anti-WD40 repeat protein 1 antibody. For quantitative analysis, immunoreactive densities were measured and quantitative real-time RT PCR was performed. WD40 repeat protein 1 expression was elevated in all the semicircular canals and utricle, two days after an acoustic overstimulation (P = 0.001). WDR1 mRNA expression was 1.34 times higher in the regeneration group compared to the normal group, but it was not statistically significant. Exceptionally, WD40 repeat protein 1 expression did not increase in the saccule of the regeneration group. Elevated WDR1 expression in the avian vestibule may have a role in the hair cell regenerating ability as in the avian cochlea. A similar mechanism of hair cell regeneration may exist in the avian cochlea and vestibule.


2019 ◽  
Vol 9 ◽  
Author(s):  
Felix M. Brehar ◽  
Mihnea P. Dragomir ◽  
George E. D. Petrescu ◽  
Radu M. Gorgan

Cell Cycle ◽  
2016 ◽  
Vol 15 (3) ◽  
pp. 413-424 ◽  
Author(s):  
Nicholas R. Lim ◽  
Yvonne Y. C. Yeap ◽  
Ching-Seng Ang ◽  
Nicholas A. Williamson ◽  
Marie A. Bogoyevitch ◽  
...  

2010 ◽  
Vol 10 (1) ◽  
pp. 169 ◽  
Author(s):  
Hong-Ju Li ◽  
Nai-You Liu ◽  
Dong-Qiao Shi ◽  
Jie Liu ◽  
Wei-Cai Yang
Keyword(s):  

Author(s):  
Kira Vanessa Blankenbach ◽  
Gennaro Bruno ◽  
Enrico Wondra ◽  
Anna Katharina Spohner ◽  
Natalie Judith Aster ◽  
...  

2015 ◽  
Vol 35 (18) ◽  
pp. 3255-3255
Author(s):  
Chi K. Leung ◽  
Koichi Hasegawa ◽  
Ying Wang ◽  
Andrew Deonarine ◽  
Lanlan Tang ◽  
...  

2005 ◽  
Vol 16 (8) ◽  
pp. 3591-3605 ◽  
Author(s):  
Shihe Li ◽  
C. Elizabeth Oakley ◽  
Guifang Chen ◽  
Xiaoyan Han ◽  
Berl R. Oakley ◽  
...  

In Aspergillus nidulans, cytoplasmic dynein and NUDF/LIS1 are found at the spindle poles during mitosis, but they seem to be targeted to this location via different mechanisms. The spindle pole localization of cytoplasmic dynein requires the function of the anaphase-promoting complex (APC), whereas that of NUDF does not. Moreover, although NUDF's localization to the spindle poles does not require a fully functional dynein motor, the function of NUDF is important for cytoplasmic dynein's targeting to the spindle poles. Interestingly, a γ-tubulin mutation, mipAR63, nearly eliminates the localization of cytoplasmic dynein to the spindle poles, but it has no apparent effect on NUDF's spindle pole localization. Live cell analysis of the mipAR63 mutant revealed a defect in chromosome separation accompanied by unscheduled spindle elongation before the completion of anaphase A, suggesting that γ-tubulin may recruit regulatory proteins to the spindle poles for mitotic progression. In A. nidulans, dynein is not apparently required for mitotic progression. In the presence of a low amount of benomyl, a microtubule-depolymerizing agent, however, a dynein mutant diploid strain exhibits a more pronounced chromosome loss phenotype than the control, indicating that cytoplasmic dynein plays a role in chromosome segregation.


2008 ◽  
Vol 28 (11) ◽  
pp. 3652-3662 ◽  
Author(s):  
Guikai Wu ◽  
Yi-Tzu Lin ◽  
Randy Wei ◽  
Yumay Chen ◽  
Zhiyin Shan ◽  
...  

ABSTRACT Spindle integrity is critical for efficient mitotic progression and accurate chromosome segregation. Deregulation of spindles often leads to structural and functional aberrations, ultimately promoting segregation errors and aneuploidy, a hallmark of most human cancers. Here we report the characterization of a previously identified human sarcoma antigen (gene located at 19p13.11), Hice1, an evolutionarily nonconserved 46-kDa coiled-coil protein. Hice1 shows distinct cytoplasmic localization and associates with interphase centrosomes and mitotic spindles, preferentially at the spindle pole vicinity. Depletion of Hice1 by RNA interference resulted in abnormal and unstable spindle configurations, mitotic delay at prometaphase and metaphase, and elevated aneuploidy. Conversely, loss of Hice1 had minimal effects on interphase centrosome duplication. We also found that both full-length Hice1 and Hice1-N1, which is composed of 149 amino acids of the N-terminal region, but not the mutant lacking the N-terminal region, exhibited activities of microtubule bundling and stabilization at a near-physiological concentration. Consistently, overexpression of Hice1 rendered microtubule bundles in cells resistant to nocodazole- or cold-treatment-induced depolymerization. These results demonstrate that Hice1 is a novel microtubule-associated protein important for maintaining spindle integrity and chromosomal stability, in part by virtue of its ability to bind, bundle, and stabilize microtubules.


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