Galpha/LGN-mediated asymmetric spindle positioning does not lead to unequal cleavage of the mother cell in 3-D cultured MDCK cells

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• 作者：Zhuoni Xiao^a ; ^b ; Qingwen Wan^a ; Quansheng Du^a ; ^{qdu@georgiahealth.edu} ; Zhen Zheng^a ; ^{zzheng@georgiahealth.edu}
• 关键词：G伪 ; the alpha subunit of heterotrimeric G proteins ; Pins ; partner of inscuteable ; LGN ; mammalian homologue of Pins ; 3-D ; three dimensional ; MDCK ; Madin Darby canine kidney ; Crb3 ; Crumb3
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：20 April, 2012
• 卷：420
• 期：4
• 页码：888-894
• 文件大小：1037 K

摘要

The position of the mitotic spindle plays a key role in spatial control of cell division. It is generally believed that when a spindle is positioned asymmetrically in a dividing cell, the resulting daughter cells are usually unequal in size due to eccentric cleavage of the mother cell. Molecular mechanisms underlying the generation of unequal sized daughter cells have been extensively studied in Drosophila neuroblast and Caenorhabditis elegans zygote where the G伪 subunit of the heterotrimeric G proteins and its binding partner - Pins in Drosophila and GPR-1/2 in C. elegans - are shown to be critical in governing spindle positioning and asymmetric cleavage of the mother cell. In mammalian system, although G伪 and LGN (mammalian Pins homolog) are also required for spindle orientation, whether they can mediate asymmetric spindle positioning or asymmetric cleavage of the mother cell is not known. Here, by artificially targeting G伪i to the apical cortex in 3-D cultured MDCK cells, we established a system where asymmetric spindle positioning can be consistently induced. Interestingly, this asymmetrically positioned spindle does not lead to asymmetric cleavage; instead it results in equal sized daughter cells. Live cell time-lapse analysis revealed that anaphase spindle elongation compensated the original asymmetric spindle positioning. Our findings demonstrate that asymmetric spindle positioning does not necessarily lead to unequal sized daughter cells in mammalian system. We discuss potential mechanisms in generating unequal sized daughter cells.