科普知识学英语 细胞分裂的“分子细节”.docVIP

Ludwig researchers Arshad Desai and Christopher Campbell, a post-doctoral fellow in his laboratory, were conducting an experiment to?parse（解析）?the molecular details of cell division about three years ago, when they engineered a mutant yeast cell as a control that, in theory, had no chance of surviving. Apparently unaware of this, the mutant thrived. Intrigued, Campbell and Desai began exploring how it had defied its predicted fate. As detailed in the current issue of Nature, what they discovered has overturned the prevailing model of how dividing cells ensure that each of their daughter cells emerge with equal numbers of chromosomes, which together package the genome. Getting the right number of chromosomes into each cell is absolutely essential to sustaining life, explains Desai, PhD, a Ludwig member at the University of California, San Diego, but it is also something that goes terribly wrong in cancer. The kinds of mistakes that occur when this process isnt functioning properly are seen in about 90% of cancers, and very frequently in advanced and drug-resistant tumors. ? Campbell and Desais study focused in particular on four interacting proteins known as the chromosomal passenger complex (CPC) that monitor the appropriate?parceling out（分配）of chromosomes. When cells initiate division, each chromosome is made of two connected, identical sister chromatids -- roughly resembling a pair of?baguettes（法国长棍面包）?joined in the middle. As the process of cell division advances, long protein ropes known as microtubules that extend from opposite ends of the cell hook up to the chromosomes to yank each of the sister chromatids in opposite directions. The microtubules attach to the chromatids via an intricate disc-like structure called the kinetochore. When the protein ropes attach correctly to the sister chromatids, pulling at each from opposing sides, they generate tension on the chromosome. One of the four proteins of the CPC, Aurora B kinase, is an enzyme that monitors that