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Heideman/NAS
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6 Q; f$ v2 i9 H3 b9 t2 K% pThe critical size model of cell division is so well established for budding yeast that, as Warren Heideman says, "it's on the wall of the Guinness Brewery." But now Tracy Laabs, Heideman (University of Wisconsin, Madison, WI), and colleagues have found that one of the pillars of the model has an alternative explanation.& Z! f' z4 s" c" n1 o4 x" ~
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The model states that cells only divide once they reach a critical size, which is why smaller daughters delay their division until they reach sizes comparable to those of their mothers. The Madison team found instead that daughters delay thanks to a daughter-localized G1 inhibitor called Ace2.After elimination of Ace2, mothers and daughters divided at the same time, so daughters divided at a smaller size than usual. An Ace2 mutant that was no longer localized to daughters also showed simultaneous division because both mothers and daughters were delayed.
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7 ^. G: \! s; {- kAce2 works at least in part by controlling levels of the G1 cyclin Cln3. In theory Ace2 could be resetting the critical size in daughters. But, says Heideman, "if you stick with critical size you have so many modifications that you are left with something very cumbersome.": q7 h) |3 M. d% G
; B ?5 z. z# N; l! w6 @He believes the cell couples growth rate and cell division rate without sensing size. "The critical size model was easily accepted by our minds because it was so elegant," he says, "but it may be hard to engineer.". W% V5 _$ p/ y3 @! g3 C
8 C5 _1 ^2 r0 E9 S$ O/ FReference:
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6 k; ~* X4 _& b$ o' x5 N9 nLaabs, T.L., et al. 2003. Proc. Natl. Acad. Sci. USA. 100:10275–10280.(Only cells with Ace2 (left) repress Cln3) |
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发表于 2009-3-6 00:55
发表于 2015-6-8 09:27
