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Science 18 May 2007: Vol. 316. no. 5827, p. 980 DOI: 10.1126/science.316.5827.980a
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Letters
When the Oil Supply Runs Out
Alfred Cavallo |
Testosterone and Male Fertility in Red Deer
Gerald A. Leblanc; William H. James; Response Montserrat Gomendio, Aurelio F. Malo, Ana J. Soler, Julian Garde, Eduardo R. S. Roldan |
How to Submit a Letter to the Editor
Technical Comment Abstracts
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COMMENT ON "A Centrosome-Independent Role for -TuRC Proteins in the Spindle Assembly Checkpoint"
Stephen S. Taylor, Kevin G. Hardwick, Kenneth E. Sawin, Sue Biggins, Simonetta Piatti, Alexey Khodjakov, Conly L. Rieder, Edward D. Salmon, Andrea Musacchio
Abstract: Müller et al. (Reports, 27 October 2006, p. 654) showed that inhibition of the -tubulin ring complex ( -TuRC) activates the spindle assembly checkpoint (SAC), which led them to suggest that -TuRC proteins play molecular roles in SAC activation. Because -TuRC inhibition leads to pleiotropic spindle defects, which are well known to activate kinetochore-derived checkpoint signaling, we believe that this conclusion is premature.
Full text at www.sciencemag.org/cgi/content/full/316/5827/982b
COMMENT ON "A Centrosome-Independent Role for -TuRC Proteins in the Spindle Assembly Checkpoint"
Beth A. A. Weaver and Don W. Cleveland
Abstract: Müller et al. (Reports, 27 October 2006, p. 654) proposed a role for microtubule nucleation in mitotic checkpoint signaling. However, their observations of spindle defects and mitotic delay after depletion of -tubulin ring complex ( -TuRC) components are fully consistent with activation of the established pathway of checkpoint signaling in response to incomplete or unstable interactions between kinetochores of mitotic chromosomes and spindle microtubules.
Full text at www.sciencemag.org/cgi/content/full/316/5827/982c
RESPONSE TO COMMENTS ON "A Centrosome-Independent Role for -TuRC Proteins in the Spindle Assembly Checkpoint"
Hannah Müller, Marie-Laure Fogeron, Verena Lehmann, Hans Lehrach, Bodo M. H. Lange
Abstract: Weaver and Cleveland and Taylor et al. contend that our data on the involvement of the -tubulin ring complex ( -TuRC) in the spindle assembly checkpoint (SAC) can be fully explained by kinetochore-derived checkpoint signaling. We maintain that (i) the interactions of -TuRC with Cdc20 and BubR1 and (ii) the activation of SAC by -TuRC depletion, in addition to the abrogation of kinetochore-microtubule interactions, argue for a more complex mechanism of SAC signaling.
Full text at www.sciencemag.org/cgi/content/full/316/5827/982d
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Science. ISSN 0036-8075 (print), 1095-9203 (online)
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