Osmani Aysha H, Davies Jonathan, Oakley C Elizabeth, Oakley Berl R, Osmani Stephen A
Department of Molecular Genetics, The Ohio State University, Columbus, Ohio 43210, USA.
Mol Biol Cell. 2003 Aug;14(8):3169-79. doi: 10.1091/mbc.e02-11-0715. Epub 2003 Apr 17.
The tinA gene of Aspergillus nidulans encodes a protein that interacts with the NIMA mitotic protein kinase in a cell cycle-specific manner. Highly similar proteins are encoded in Neurospora crassa and Aspergillus fumigatus. TINA and NIMA preferentially interact in interphase and larger forms of TINA are generated during mitosis. Localization studies indicate that TINA is specifically localized to the spindle pole bodies only during mitosis in a microtubule-dependent manner. Deletion of tinA alone is not lethal but displays synthetic lethality in combination with the anaphase-promoting complex/cyclosome mutation bimE7. At the bimE7 metaphase arrest point, lack of TINA enhanced the nucleation of bundles of cytoplasmic microtubules from the spindle pole bodies. These microtubules interacted to form spindles joined in series via astral microtubules as revealed by live cell imaging. Because TINA is modified and localizes to the spindle pole bodies at mitosis, and lack of TINA causes enhanced production of cytoplasmic microtubules at metaphase arrest, we suggest TINA is involved in negative regulation of the astral microtubule organizing capacity of the spindle pole bodies during metaphase.
构巢曲霉的tinA基因编码一种能以细胞周期特异性方式与NIMA有丝分裂蛋白激酶相互作用的蛋白质。粗糙脉孢菌和烟曲霉中编码有高度相似的蛋白质。TINA和NIMA在间期优先相互作用，且在有丝分裂期间会产生更大形式的TINA。定位研究表明，TINA仅在有丝分裂期间以微管依赖的方式特异性定位于纺锤极体。单独缺失tinA并不致命，但与后期促进复合物/细胞周期体突变bimE7结合时表现出合成致死性。在bimE7中期停滞点，缺乏TINA会增强纺锤极体产生的细胞质微管束的成核作用。活细胞成像显示，这些微管相互作用形成通过星体微管串联连接的纺锤体。由于TINA在有丝分裂时被修饰并定位于纺锤极体，且缺乏TINA会导致中期停滞时细胞质微管的产生增加，我们认为TINA参与中期纺锤极体星体微管组织能力的负调控。
