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BubR1, but not Mad2, is required for recruiting and localizing of Fzy to the kinetochores in D. melanogaster

Lookup NU author(s): Deyu Li, Emeritus Professor Michael Whitaker, Dr Jun-yong Huang

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Abstract

Mad2 and BubR1, two important spindle checkpoint proteins, have been reported to inhibit anaphase promoting complex/cyclosome (APC/C) activity by binding to its activator Cdc20 (or Fzy in Drosophila), which results in suspension of the metaphase/anaphase transition until all the kinetochores are properly attached to microtubules and the sister chromatids aligned properly at metaphase plate. However, it is still unclear how these three proteins interact on kinetochores in time and space to generate this inhibitory signal. Here we report that the dynamic distribution and localization of GFP-Mad2 in Drosophila syncytial embryos is consistent with that reported in other systems though in addition it predominantly localizes with the nuclear regions throughout the cell cycle. Drosophila Mad2 associates with kinetochores at prophase and starts to disappear from early metaphase kinetochores. Interestingly, we found that the dynamic distribution of average fluorescent intensities of CFP-Mad2 and YFP-Fzy in the nucleus regions oscillates out of phase with each other in transgenic Drosophila syncytial embryos that co-express these two proteins. Surprisingly, Mad2 does not appear to be an essential protein for mitotic progression; flies without Mad2 (Mutant: EY21687) develop normally. Furthermore, we have found the recruitment and kinetochore localization of Fzy is dependent on BubR1, but not Mad2, when we examined the localizations of GFP-Fzy in Mad2 or BubR1 null mutant embryos and neuroblast cells.


Publication metadata

Author(s): Li D, Karess R, Whitaker M, Huang J-Y

Publication type: Conference Proceedings (inc. Abstract)

Conference Name: 48th Annual Drosophila Research Conference

Year of Conference: 2007

Pages: 37, 165C

Publisher: The Genetics Society of America

URL: http://www.drosophila-conf.org/2007/PDF/Dros07Volume.pdf

Sponsor(s): The Genetics Society of America


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