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Arabidopsis Homologs of Nucleus- and Phragmoplast-Localized Kinase 2 and 3 and Mitogen-Activated Protein Kinase 4 Are Essential for Microtubule Organization

机译:核和膜质体定位激酶2和3和有丝分裂原激活的蛋白激酶4的拟南芥同源物是微管组织必不可少的。

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摘要

A double homozygous recessive mutant in the Arabidopsis thaliana homologs of nucleus- and phragmoplast-localized kinase 2 (ANP2) and 3 (ANP3) genes and a homozygous recessive mutant in the mitogen-activated protein kinase 4 (MPK4) gene of Arabidopsis exhibit deficiencies in the overall microtubule (MT) organization, which result in abnormal cell growth patterns, such as branching of root hairs and swelling of diffusely growing epidermal cells. Genetic, pharmacological, molecular, cytological, and biochemical analyses show that the major underlying mechanism for these phenotypes is excessive MT stabilization manifested in both mutants as heavy MT bundling, disorientation, and drug stability. The above defects in MAPK signaling result in the adverse regulation of members of the microtubule-associated protein (MAP65) protein family, including strongly diminished phosphorylation of MAP65-1. These data suggest that ANP2/ANP3, MPK4, and the microtubule-associated protein MAP65-1, a putative target of MPK4 signaling, are all essential for the proper organization of cortical microtubules in Arabidopsis epidermal cells.
机译:拟南芥中核和原生质膜激酶2(ANP2)和3(ANP3)基因的一个纯合隐性突变体和有丝分裂原的拟南芥丝裂蛋白激酶4(MPK4)基因中的一个纯合性隐性突变体表现出缺陷整个微管(MT)组织,导致异常的细胞生长方式,例如根毛分支和扩散生长的表皮细胞肿胀。遗传,药理,分子,细胞学和生化分析表明,这些表型的主要潜在机制是MT的过度稳定,这两个突变体均表现为重度MT束缚,方向混乱和药物稳定性。 MAPK信号转导中的上述缺陷导致对微管相关蛋白(MAP65)蛋白家族成员的不利调节,包括MAP65-1磷酸化的强烈降低。这些数据表明,ANP2 / ANP3,MPK4和微管相关蛋白MAP65-1(MPK4信号的推定靶标)对于拟南芥表皮细胞中皮质微管的正确组织都是必不可少的。

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