Spatial regulation of the spindle assembly checkpoint in Aspergillus nidulans.

H. Edgerton-Morgan1,2, T. Nayak1, and B.R. Oakley2

Author address: 

Molecular Genetics, The Ohio State University, Columbus, OH. 2Molecular Biosciences, University of Kansas, Lawrence, KS

Abstract: 

The Aspergillus nidulans gamma-tubulin mutation mipAD159 causes a nuclear autonomous failure of inactivation of the anaphase promoting complex/cyclosome (APC/C) removing affected nuclei from the cell cycle (Nayak et al., 2010, J. Cell Biol. 190:317-330). This raised the question as to why the APC/C was not inactivated in mitosis in those nuclei by the spindle assembly checkpoint (SAC). MipAD159 causes additional defects in mitotic and cell cycle regulation without inhibiting microtubule nucleation (Prigozhina et al., 2004, Mol. Biol. Cell, 15:1374-1386) suggesting that gamma-tubulin may have additional roles in mitotic regulation. To determine if mipAD159 affects the SAC, we have tagged and imaged A. nidulans homologs of four components of the SAC: Mad2, Mps1, Bub3, and BubR1. The four proteins were spatially separated in interphase until they came together at mitotic onset forming the mitotic checkpoint complex. This implies that SAC activity is controlled in part by regulation of the locations of its components. In strains carrying mipAD159, BubR1 failed to accumulate at the SPB/K in some nuclei. BubR1 has two APC/C recognition sequences and is likely destroyed in these nuclei by a constitutively active APC/C, preventing activation of the SAC. Mad2, Bub3 and Mps1 localized to the SPB/K normally when BubR1 was absent and they, thus, do not depend on BubR1 for SPB/K localization. We have found that, unlike BubR1, Bub3 and Mad2, Mps1 is essential for viability. This indicates that Mps1 has an essential function independent of the SAC. Supported by NIH grant GM031837.
2011

abstract No: 

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Full conference title: 

26th Fungal Genetics Conference
    • Fungal Genetics Conference 26th (2005)