Sveiczer A, Novak B, Mitchison J M
Department of Agricultural Chemical Technology, Technical University of Budapest, Szt. Gellert ter 4, Hungary.
J Cell Sci. 1999 Apr;112 ( Pt 7):1085-92. doi: 10.1242/jcs.112.7.1085.
Fission yeast cells tolerate the total absence of the cdc25 mitotic inducer in two cases, either in cdc2-3w or in wee1 genetic backgrounds. In the cdc2-3w cdc25Delta double mutant, the rate-limiting step leading to mitosis is reaching a critical size. However, the size control of this mutant operates in late G2, which is different from wild-type (WT) cells. This fact suggests that in WT the rate-limiting molecular process during the G2 timer is the Tyr15 dephosphorylation of cdc2, for which the cdc25 phosphatase (together with its back-up, pyp3) is dependent. In the wee1-50 cdc25Delta mutant, the population splits into different clusters, all lacking mitotic size control. This strain maintains size homeostasis by a novel method, which is random movement of the cells from one cluster to another in the successive generations. These cells should normally have a 'minimal cycle', a 'timer' with short G1 and G2 phases. However, very often the cells abort mitosis, possibly at an early event and return back to early G2, thus lengthening their cycles. The inability of these cells to start anaphase might be caused by the absence of the main mitotic regulators (wee1 and cdc25) and the improper regulation of their back-up copies (mik1 and pyp3, respectively).
裂殖酵母细胞在两种情况下能够耐受完全缺失cdc25有丝分裂诱导因子，即处于cdc2-3w或wee1基因背景中。在cdc2-3w cdc25Δ双突变体中，导致有丝分裂的限速步骤是达到临界大小。然而，该突变体的大小控制在G2晚期起作用，这与野生型（WT）细胞不同。这一事实表明，在WT中，G2期定时器期间的限速分子过程是cdc2的Tyr15去磷酸化，而cdc25磷酸酶（及其备份pyp3）对此是必需的。在wee1-50 cdc25Δ突变体中，细胞群体分裂成不同的簇，所有簇都缺乏有丝分裂大小控制。该菌株通过一种新方法维持大小稳态，即细胞在连续几代中从一个簇随机移动到另一个簇。这些细胞正常情况下应该有一个“最小周期”，一个G1期和G2期较短的“定时器”。然而，这些细胞经常在有丝分裂早期中止，可能在早期事件时就回到G2早期，从而延长了它们的周期。这些细胞无法开始后期可能是由于主要有丝分裂调节因子（wee1和cdc25）的缺失以及它们的备份拷贝（分别为mik1和pyp3）的调节不当所致。
