Vascular stem cell maintenance is regulated by a peptide signaling involving Tracheary Element Differentiation Inhibitory Factor (TDIF) and Receptor TDR/PXY (Phloem intercalated with Xylem) and co-receptor BAK1 (BRI1-associated receptor kinase1). The regulatory mechanism of this signaling pathway is largely unknown despite its importance in stem cell maintenance in the vascular meristem. We report that activation of a NAC domain transcription factor XVP leads to precocious Xylem differentiation, disruption of Vascular Patterning, and reduced cell numbers in vascular bundles. We combined molecular and genetic studies to elucidate the biological functions of XVP. XVP is expressed in the cambium, localized on the plasma membrane and forms a complex with TDIF co-receptors PXY-BAK1. Simultaneous mutation of XVP and its close homologous NAC048 enhances TDIF signaling. In addition, genetics analysis indicated that XVP promotes xylem differentiation through a known master regulator VASCULAR-RELATED NAC-DOMAIN6 (VND6). Expression analyses indicate that XVP activates CLAVATA3/ESR (CLE)-related protein 44 (CLE44), the coding gene of TDIF, whereas TDIF represses XVP expression, suggesting a feedback mechanism. Therefore, XVP functions as a negative regulator of the TDIF-PXY module and fine-tunes TDIF signaling in vascular development. These results shed new light on the mechanism of vascular stem cell maintenance.

中文翻译：

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膜相关的NAC域转录因子XVP与TDIF协同受体相互作用，并调节血管分生组织的活性。

血管干细胞的维持是由涉及气管元素分化抑制因子（TDIF）和受体TDR / PXY（韧皮部与木质部插入）和共受体BAK1（BRI1相关受体激酶1）的肽信号调控的。尽管该信号通路在维系分生组织的干细胞维持中具有重要作用，但其调控机制在很大程度上尚不清楚。我们报告的激活NAC域转录因子XVP导致性早熟木质部分化，血管模式的破坏和减少血管束中的细胞数。我们结合了分子和遗传研究，以阐明XVP的生物学功能。XVP在形成层中表达，定位在质膜上，并与TDIF共受体PXY-BAK1形成复合物。XVP及其紧密同源NAC048的同时突变可增强TDIF信号传导。另外，遗传学分析表明，XVP通过已知的主调控因子VASCULAR-NALATED NAC-DOMAIN6（VND6）促进木质部分化。表达分析表明XVP激活CLIFATA3 / ESR（CLE）相关蛋白44（CLE44），它是TDIF的编码基因，而TDIF则抑制XVP的表达，提示了一种反馈机制。因此，XVP充当TDIF-PXY模块的负调节剂，并微调TDIF在血管发育中的信号传导。这些结果为维持血管干细胞的机制提供了新的思路。表达分析表明XVP激活CLIFATA3 / ESR（CLE）相关蛋白44（CLE44），它是TDIF的编码基因，而TDIF则抑制XVP的表达，提示了一种反馈机制。因此，XVP充当TDIF-PXY模块的负调节剂，并微调TDIF在血管发育中的信号传导。这些结果为维持血管干细胞的机制提供了新的思路。表达分析表明XVP激活CLIFATA3 / ESR（CLE）相关蛋白44（CLE44），它是TDIF的编码基因，而TDIF则抑制XVP的表达，提示了一种反馈机制。因此，XVP充当TDIF-PXY模块的负调节剂，并微调TDIF在血管发育中的信号传导。这些结果为维持血管干细胞的机制提供了新的思路。