郁飞等《Plant Cell》2022年

论文题目：MOR1/MAP215 acts synergistically with katanin to control cell division and anisotropic cell elongation in Arabidopsis

论文作者：Yu Chen，Xiayan Liu，Wenjing Zhang，Jie Li，Haofeng Liu,Lan Yang，Pei Lei，Hongchang Zhang，Fei Yu

论文摘要：The MAP215 family of microtubule (MT) polymerase/nucleation factors and the MT severing enzyme katanin are widely conserved microtubule-associated proteins (MAPs) across the plant and animal kingdoms. However, how these two essential MAPs coordinate to regulate plant MT dynamics and development remains unknown. Here, we identified novel hypomorphic alleles of MICROTUBULE ORGANIZATION 1 (MOR1), encoding the Arabidopsis thaliana homolog of MAP215, in genetic screens for mutants oversensitive to the MT-destabilizing drug propyzamide. Live imaging in planta revealed that MOR1-green fluorescent protein (GFP) predominantly tracks the plus-ends of cortical MTs in interphase cells and labels preprophase band, spindle and phragmoplast MT arrays in diving cells. Remarkably, MOR1 and KATANIN 1 (KTN1), the p60 subunit of Arabidopsis katanin, act synergistically to control the proper formation of plant-specific MT arrays, and consequently, cell division and anisotropic cell expansion. Moreover, MOR1 physically interacts with KTN1 and promotes KTN1-mediated severing of cortical MTs. Our work establishes the Arabidopsis MOR1-KTN1 interaction as a central functional node dictating MT dynamics and plant growth and development.

微管(MT)聚合酶/成核因子MAP215家族和MT切割katanin是在动植物中广泛保守的微管相关蛋白(MAPs)。然而，目前尚不清楚这两个重要的MAP如何协同调控植物微管动态和生长发育。本研究中，通过筛选微管解聚药物超敏感突变体，获得了编码拟南芥MAP215的MOR1基因的新的非致死突变体mor1-10，构建了稳定表达有功能MOR1-GFP融合蛋白的转基因植株。植物活体显像显示，在分裂间期的细胞中，MOR1-GFP定位于周质微管，并在微管正端富集；在分裂期细胞中，MOR1-GFP在早前期带、纺锤体和成膜体微管阵列上均匀分布。进一步研究发现，遗传和功能互作研究表明，MOR1与KTN1在间期细胞中协同调控细胞各向异性扩张，在分裂期细胞中协同调控细胞分裂平面的精确定位。进一步研究发现，MOR1与KTN1之间存在直接的物理互作，促进KTN1被招募至微管切割位点，进而促进KTN1介导的微管切割。该研究揭示了MOR1-KTN1这一微管动态调控的关键功能单元，增进了对植物微管结合蛋白互作机制和微管动态调控机理的认识。

文章链接：https://academic.oup.com/plcell/advance-article-abstract/doi/10.1093/plcell/koac147/6586806?redirectedFrom="fulltext"