Myosin-II reorganization during mitosis is controlled temporally by its dephosphorylation and spatially by Mid1 in fission yeast.
Myosin-II reorganization during mitosis is controlled temporally by its dephosphorylation and spatially by Mid1 in fission yeast.
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DOI：
10.1083/jcb.200402097
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发表时间：
2004-06-07
期刊：
影响因子：
--
通讯作者：
Mabuchi I
中科院分区：
文献类型：
--
作者：
Motegi F;Mishra M;Balasubramanian MK;Mabuchi I
许多真核生物的胞质分裂需要肌动球蛋白收缩环。在这里，我们证明了在分裂酵母中，肌球蛋白-II重链MyO2最初通过其COOH末端的134个氨基酸积累在分裂位点，而不依赖于F-肌动蛋白。COOH-末端区域可以在G2早期到达分裂位置，而完整的MyO2在有丝分裂早期可以到达。Myo2 COOH末端的Ser1444是一个磷酸化位点，在有丝分裂早期被去磷酸化。Myo2 S1444A过早地聚集在未来的分裂部位，并促进F-肌动蛋白环的形成，即使在间期也是如此。Myo2的积累需要在适当的环位置发挥作用的苯丙素同系物MID1。Myo2在细胞裂解产物中与MID1相互作用，这种相互作用被Myo2中的S1444D突变所抑制。我们的结果表明，Myo2的去磷酸化将COOH末端区域从分子内抑制中解放出来。随后，去磷酸化的Myo2被MID1锚定在内侧皮质，并与F-肌动蛋白合作促进环组装。
Cytokinesis in many eukaryotes requires an actomyosin contractile ring. Here, we show that in fission yeast the myosin-II heavy chain Myo2 initially accumulates at the division site via its COOH-terminal 134 amino acids independently of F-actin. The COOH-terminal region can access to the division site at early G2, whereas intact Myo2 does so at early mitosis. Ser1444 in the Myo2 COOH-terminal region is a phosphorylation site that is dephosphorylated during early mitosis. Myo2 S1444A prematurely accumulates at the future division site and promotes formation of an F-actin ring even during interphase. The accumulation of Myo2 requires the anillin homologue Mid1 that functions in proper ring placement. Myo2 interacts with Mid1 in cell lysates, and this interaction is inhibited by an S1444D mutation in Myo2. Our results suggest that dephosphorylation of Myo2 liberates the COOH-terminal region from an intramolecular inhibition. Subsequently, dephosphorylated Myo2 is anchored by Mid1 at the medial cortex and promotes the ring assembly in cooperation with F-actin.
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DOI：
10.1083/jcb.137.6.1309
发表时间：
1997-06-16
期刊：
The Journal of cell biology
影响因子：
--
作者：
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影响因子：
7.8
作者：
MCCOLLUM, D;BALASUBRAMANIAN, MK;PELCHER, LE;HEMMINGSEN, SM;GOULD, KL
通讯作者：
GOULD, KL
DOI：
10.1083/jcb.143.6.1603
发表时间：
1998-12-14
期刊：
The Journal of cell biology
影响因子：
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作者：
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3.3
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通讯作者：
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影响因子：
6.6
作者：
Arai, R;Nakano, K;Mabuchi, I
通讯作者：
Mabuchi, I