Abstract
AbstractSpatiotemporal control over developmental programs is vital to all organisms. Here we show that cytokinin (signaling) deficiency leads to early secondary cell wall (SCW) formation in Arabidopsis inflorescence stem that associates with precocious upregulation of a SCW transcriptional cascade controlled by NAC TFs (NSTs). We demonstrate that cytokinin signaling through the AHK2/3 and the ARR1/10/12 suppresses the expression of severalNSTsand SCW formation in the apical portions of stems. Exogenous cytokinin application reconstituted both proper development and apical-basal gradient ofNST1andNST3in a cytokinin biosynthesis-deficient mutant. We show thatAHK2andAHK3required functionalNST1orNST3to control SCW initiation in the interfascicular fibers, further evidencing that cytokinins act upstream ofNSTs transcription factors. The premature onset of a rigid SCW biosynthesis and altered expression ofNST1/3andVND6/7due to cytokinin deficiency led to the formation of smaller tracheary elements (TEs) and impaired hydraulic conductivity. We conclude that cytokinins downregulateNSTsto inhibit premature SCW formation in the apical part of the inflorescence stem, facilitating thus the development of fully functional TEs and interfascicular fibers.Summary statementCytokinins attenuate premature secondary cell wall (SCW) formation via downregulating the expression of NAC TFs, the master switches of SCW transcriptional cascade, thus affecting the tracheary elements size and conductivity.
Publisher
Cold Spring Harbor Laboratory