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. 2013 Aug 1;24(15):2419–2430. doi: 10.1091/mbc.E13-03-0126

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© 2013 Yang et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 7: — Tethering Clb2 inside the nucleus results in nuclear fission failure. (A) Schematic of optogenetic nuclear recruitment of Clb2, and Clb2 localization under 750- and 650-nm light (inset). (B) Sequestering Clb2 to nucleus (PhyB-HTB2) results in nuclear fission defect. Combined phase and fluorescence time-course images (3-min interval) when Clb2 is not recruited to the nucleus (750-nm light; top and Supplemental Movie S2) vs. when Clb2 is recruited to the nucleus (with 650-nm light; bottom and Supplemental Movies S3 and S4). Red channel represents the nucleus (PhyB-mCherry-HTB2), and the green channel represents the spindle pole body (Spc42-GFP). (C) Kymograph of spindle pole dynamics when Clb2 is unrecruited (system is OFF, left) vs. when Clb2 is recruited to the nucleus (system is ON, right) with a time interval of 3 min. (D) The nuclear fission failure is rescued by adding an extra untagged copy of CLB2, suggesting that nuclear fission failure is likely due to cytoplasmic Clb2 depletion. The average cell size in different strains is shown as the inset.