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. 2016 Jun 2;44(16):7722–7741. doi: 10.1093/nar/gkw506

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© The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — HOP1 overexpression largely restores meiotic arrest, Mek1 activation, Mek1 localization and delayed Cdc5 production in zip1 pch2. Western blot analysis of the indicated proteins and meiotic kinetics of (A and B) wild type, (C and D) zip1 and (E and F) zip1 pch2 transformed with empty vector (pRS426) or high-copy HOP1 (R1692). Strains are: DP421 (wild type), DP422 (zip1) and DP1029 (zip1 pch2). (G) Analysis of Mek1 phosphorylated forms in ndt80-arrested strains. The black arrowhead marks the Mec1/Tel1-dependent band and the white arrowheads point to the forms resulting from Mek1 autophosphorylation (8). Strains are: DP428 (zip1) and DP881 (zip1 pch2), transformed with pRS426 (empty vector) or R1692 (OE-HOP1). (H) Analysis of Mek1 localization by immunofluorescence of spread meiotic chromosomes using anti-GFP antibodies. Representative nuclei are shown. Strains are DP582 (zip1) and DP1111 (zip1 pch2).