The molecular mechanisms of a regulatory pathway involved in plant cell division

NACK-PQR途径由烟草中的NACK1激动素蛋白、NPK1 MAPKKK、NQK1 MAPKK和NRK1/NTF6 MAPK组成，是植物细胞质分裂的关键调节因子。在胞质分裂过程中，NACK1和NPK1通过直接结合而被特异性地激活，然而，这些蛋白之间的相互作用是如何调节的还有待确定。在这里，我们报告了CDK在中期之前负向调节NACK-PQR途径。利用烟草细胞，我们证明了细胞周期蛋白依赖性蛋白激酶(CDKs)在中期之前对NPK1和NACK1进行了磷酸化。这种磷酸化通过抑制这两种蛋白质之间的相互作用来阻止向胞质分裂的转变。如果不能在中期使CDKs失活，就会阻止这两种蛋白的去磷酸化，导致不完全有丝分裂。用拟南芥NACK1(也称为Hinkel)进行的实验表明，磷酸化的NACK1不能介导胞质分裂。因此，CDKs及时和协调的磷酸化以及细胞动力学调节因子从前期到后期的去磷酸化对于胞质分裂的适当开始和/或进展至关重要。

The NACK-PQR pathway, which is composed by NACK1 kinesin-like protein, NPK1 MAPKKK, NQK1 MAPKK and NRK1/NTF6 MAPK in tobacco, is known as a key regulator for plant cytokinesis. This pathway is specifically activated during cytokinesis via the direct binding between NACK1 and NPK1, however, it remains to be determined how the interaction of these proteins is regulated. Here, we report that CDKs negatively regulate the NACK-PQR pathway before metaphase. Using tobacco cells, we demonstrated that cyclin-dependent kinases (CDKs) phosphorylate both NPK1 and NACK1 before metaphase. Such phosphorylation prevents the transition to cytokinesis via inhibition of interactions between these two proteins. Failure to inactivate CDKs after metaphase prevents dephosphorylation of these two proteins, causing incomplete mitosis. Experiments with Arabidopsis NACK1 (known also as HINKEL) revealed that phosphorylated NACK1 fails to mediate cytokinesis. Thus, timely and coordinated phosphorylation by CDKs and dephosphorylation of cytokinetic regulators from prophase to anaphase are critical for the appropriate onset and/or progression of cytokinesis.