Microtubules play pivotal roles in establishing trichome branching patterns, which is a model system for studying cell-shape control in Arabidopsis (Arabidopsis thaliana). However, the signaling pathway that regulates microtubule reorganization during trichome branching remains poorly understood. In this study, we report that MICROTUBULE-DESTABILIZING PROTEIN25 (MDP25) is involved in GLABRA3 (GL3)-mediated trichome branching by regulating microtubule stability. Loss of MDP25 function led to excessive trichome branching, and this phenotype in mdp25 could not be rescued by the MDP25 K7A or MDP25 K18A mutated variants. Pharmacological treatment and live-cell imaging revealed increased microtubule stability in the mdp25 mutant. Furthermore, the microtubule collar observed during trichome branching remained more intact in mdp25 compared to the WT under oryzalin treatment. Results of genetic assays further demonstrated that knocking out MDP25 rescued the reduced branching phenotype of gl3 trichomes. In gl3 trichomes, normal microtubule organization was disrupted, and microtubule stability was significantly compromised. Moreover, GL3 physically bound to the MDP25 promoter, thereby inhibiting its expression. Overexpression of GL3 negated the effects of PMDP25-driven MDP25 or its mutant proteins on trichome branching and microtubules in the mdp25 background. Overall, our study uncovers a mechanism by which GL3 inhibits MDP25 transcription, thereby influencing microtubule stability and regulating trichome branching. This mechanism provides a connection between early regulatory components and microtubules during trichome development.

中文翻译：

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GLABRA3介导的毛状体分支需要 MICROTUBULE 不稳定PROTEIN25的转录抑制


微管在建立毛状体分支模式中起关键作用，这是研究拟南芥 （Arabidopsis thaliana） 细胞形状控制的模型系统。然而，在毛状体分支过程中调节微管重组的信号通路仍然知之甚少。在这项研究中，我们报道了微管不稳定PROTEIN25 （MDP25） 通过调节微管稳定性参与 GLABRA3 （GL3） 介导的毛状体分支。MDP25 功能丧失导致过度的毛状体分支，MDP25 中的这种表型无法被 MDP25 K7A 或 MDP25 K18A 突变变体挽救。药物治疗和活细胞成像显示 mdp25 突变体的微管稳定性增加。此外，与谷维素处理下的 WT 相比，在毛状体分支期间观察到的微管环在 mdp25 中保持更完整。基因检测结果进一步表明，敲除 MDP25 挽救了 gl3 毛状体的分支表型减少。在 gl3 毛状体中，正常的微管组织被破坏，微管稳定性受到显着损害。此外，GL3 与 MDP25 启动子物理结合，从而抑制其表达。GL3 的过表达抵消了 PMDP25 驱动的 MDP25 或其突变蛋白对 mdp25 背景中毛状体分支和微管的影响。总体而言，我们的研究揭示了 GL3 抑制 MDP25 转录的机制，从而影响微管稳定性并调节毛状体分支。这种机制在毛状体发育过程中提供了早期调节成分和微管之间的联系。