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. 2014 Mar 15;127(6):1346–1356. doi: 10.1242/jcs.146373

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© 2014. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 8. — The convergence of multiple pathways to control Cdc2–cyclin-B activity. (A) Alignment of TOR and TOR-related kinases. Conserved residues are highlighted in bold. The key Torin-interacting tryptophan is shown in cyan. The Torin1 resistant tor2-G2040D is shown in red. (B) A model suggesting that when Torin1 inhibits TORC1, Wee1 levels decline. This traps Cdc2–cyclin-B in its active conformation, driving entry into mitosis at a reduced cell size. The presence of molecule X is implied by advanced mitosis in torin1-treated plo1.S402A cdr2::ura4⁺ double mutants. Insert: in contrast to rapamycin, regulation of either Wee1 (1) or Cdc25 (2) is sufficient to advance mitotic onset following the strong Torin1-induced TOR inhibition.