Tanaka K, Petersen J, MacIver F, Mulvihill D P, Glover D M, Hagan I M
School of Biological Sciences, 2.205 Stopford Building, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK.
EMBO J. 2001 Mar 15;20(6):1259-70. doi: 10.1093/emboj/20.6.1259.
Plo1-associated casein kinase activity peaked during mitosis before septation. Phosphatase treatment abolished this activity. Mitotic Plo1 activation had a requirement for prior activation of M-phase promoting factor (MPF), suggesting that Plo1 does not act as a mitotic trigger kinase to initiate MPF activation during mitotic commitment. A link between Plo1 and the septum initiating network (SIN) has been suggested by the inability of plo1 Delta cells to septate and the prolific septation following plo1(+) overexpression. Interphase activation of Spg1, the G protein that modulates SIN activity, induced septation but did not stimulate Plo1-associated kinase activity. Conversely, SIN inactivation did not affect the mitotic stimulation of Plo1-associated kinase activity. plo1.ts4 cells formed a misshapen actin ring, but rarely septated at 36 degrees C. Forced activation of Spg1 enabled plo1.ts4 mutant cells, but not cells with defects in the SIN component Sid2, to convert the actin ring to a septum. The ability of plo1(+) overexpression to induce septation was severely compromised by SIN inactivation. We propose that Plo1 acts before the SIN to control septation.
与Plo1相关的酪蛋白激酶活性在有丝分裂期间隔膜形成之前达到峰值。磷酸酶处理消除了这种活性。有丝分裂期Plo1的激活需要前期M期促进因子（MPF）的激活，这表明Plo1在有丝分裂起始过程中并非作为启动MPF激活的有丝分裂触发激酶。plo1Δ细胞无法形成隔膜以及plo1(+)过表达后大量形成隔膜，这表明Plo1与隔膜起始网络（SIN）之间存在联系。调节SIN活性的G蛋白Spg1在间期的激活诱导了隔膜形成，但并未刺激与Plo1相关的激酶活性。相反，SIN失活并不影响有丝分裂期对与Plo1相关激酶活性的刺激。plo1.ts4细胞形成了畸形的肌动蛋白环，但在36℃时很少形成隔膜。强制激活Spg1可使plo1.ts4突变细胞（但不包括SIN组分Sid2有缺陷的细胞）将肌动蛋白环转变为隔膜。SIN失活严重损害了plo1(+)过表达诱导隔膜形成的能力。我们提出Plo1在SIN之前发挥作用以控制隔膜形成。
