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Summary Plant secondary growth drives stem thickening and biomass accumulation, but its regulation is not yet fully understood.We have identified a novel semi‐dominant mutant,rbe‐d, characterized by a significant reduction in cambium cells and a complete absence of secondary growth in interfascicular regions in the stem. Gene cloning experiments indicated that the activation of the C2H2 zinc finger transcription factor, AT5G06070/RABBIT EARS (RBE), is responsible for therbe‐dphenotype.Transgenic analysis confirmed that overexpression of RBE represses secondary growth, while therbe‐2mutant increased the width of the interfascicular cambium‐derived (ICD) region. TheRBEgene is expressed in the procambium and cambium regions. Transcriptomic analysis showed that genes of the tracheary element differentiation inhibitory factor‐phloem intercalated with xylem (TDIF‐PXY) central regulatory pathway are repressed in therbe‐dmutant plants. Biochemical analyses confirmed that RBE binds directly to the promoter of WUSCHEL‐related homeobox (WOX4), a TDIF‐PXY downstreamWOXgene that regulates cambium cell proliferation. Moreover, genetic analysis confirmed thatWOX4is epistatic toRBEin secondary growth.Our results indicate that RBE inhibits cambium proliferation and thereby impacts secondary growth by directly repressingWOX4. These findings offer valuable new insight into the regulation of secondary growth in the Arabidopsis stem. 

Summary Vascular bundles transport water and photosynthate to all organs, and increased bundle number contributes to crop lodging resistance. However, the regulation of vascular bundle formation is poorly understood in the Arabidopsis stem.We report a novel semi‐dominant mutant with high vascular activity,hva‐d, showing increased vascular bundle number and enhanced cambium proliferation in the stem. The activation of a C2H2 zinc finger transcription factor,AT5G27880/HVA, is responsible for thehva‐dphenotype. Genetic, biochemical, and fluorescent microscopic analyses were used to dissect the functions of HVA.HVA functions as a repressor and interacts with TOPLESS via the conserved Ethylene‐responsive element binding factor‐associated Amphiphilic Repression motif. In contrast to the HVA activation line, knockout ofHVAfunction with a CRISPR‐Cas9 approach or expression of HVA fused with an activation domain VP16 (HVA‐VP16) resulted in fewer vascular bundles. Further, HVA directly regulates the expression of the auxin transport efflux facilitatorPIN1, as a result affecting auxin accumulation. Genetics analysis demonstrated that PIN1 is epistatic to HVA in controlling bundle number.This research identifies HVA as a positive regulator of vascular initiation through negatively modulating auxin transport and sheds new light on the mechanism of bundle formation in the stem.