Abstract text: Xylem vessel is an essential constituent of the vascular system in land plants. In Arabidopsis, the NAC transcription factor VND7 works as the master regulator of xylem vessel differentiation, through the induction of genes for lignified secondary cell wall biosynthesis and programmed cell death. The seiv mutants exhibit defects in VND7-induced ectopic xylem vessel differentiation, as well as endogenous xylem vessel functionality. One of the mutants, seiv9, has a dominant mutation of U-box E3 ligase involved in the protein ubiquitination, suggesting the importance of ubiquitination of VND7 for xylem vessels. Here, we newly demonstrated that seiv9 showed hypersusceptible to Colletotrichum species along with impaired hypersensitive-response cell death, and suppressed immune responses to the bacterial elicitor flg22, including reduced the MAP kinase (MAPK) activation and ROS burst. Moreover, the VND family proteins were found to be phosphorylated by MAPKs, which is required for xylem differentiation. These results indicate that VND7 activity is controlled not only directly by protein ubiquitination but also by protein phosphorylation via the ubiquitination-based regulation of MAPK activity. Together, our findings highlight the sophisticated control of VND7 protein modification to enable plants to regulate xylem functionality in response to biotic stress.