Abstract
The overexpression of miR319 in plants results in delayed senescence, and high levels of miR319-targeted TCP4 transcription factor cause premature onset of this process. However, the underlying mechanisms of this pathway remain elusive. Here, we found that miR319 overexpression results in a decrease in TCP4 abundance and secondary cell wall formation in the stem. Conversely, constitutive expression of miR319-resistant TCP4 promotes secondary cell wall formation, indicating that miR319-mediated TCP4 controls secondary cell wall formation during development. Further analysis revealed that TCP4 might directly bind the promoter of VND7 to activate its expression, which triggers the expression of a VND7 transcriptional network associated with secondary cell wall biosynthesis and programmed cell death and accelerates vessel formation. In addition, the development process gradually increased TCP4 expression. These results suggest that miR319 and its target TCP4 can act as switches that turn on secondary cell wall synthesis and programmed cell death.