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mutants of atm, a gene required for the DNA damage checkpoint) did not cause
any tumor formation upon transplantation. These results led the authors to propose
that the defective genomic stability upon centrosome dysfunction is not the cause
of tumor formation; instead, centrosome dysfunction causes tumors through dis-
turbing asymmetric stem cell divisions (Castellanos et al. 2008 ).
Because of its duplication mechanism during centriole biogenesis, the centro-
some displays inherent asymmetry in cellular processes. Now we know several
examples in which centrosome asymmetry is integrated into a higher level of
asymmetry, i.e., fate, during stem cell divisions. While it is tempting to speculate
that centrosome asymmetry is a universal mechanism for cells to divide asym-
metrically, such assumptions and underlying mechanisms remain to be elucidated.
Acknowledgment The authors wish to acknowledge financial support from Chicago Biomedical
Consortium from The Searle Funds at The Chicago Community Trust to J.C., Postdoctoral
Fellowship from the Training Program in Organogenesis (T-32-HD007505) to T.M.R., and
MacArthur Foundation to Y.M.Y.
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