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Abstract

Abstract Secondary growth contributes to the production of most of the plant biomass by deposition of cell-wall material within the secondary xylem. Secondary xylem not only functions as a conduit transporting water and minerals throughout plant body, but also provides mechanical support for maintaining plant architecture. In vascular plants, secondary xylem differentiates from the vascular cambium, which in parallel generates phloem in the opposite direction and, thereby, driving radial plant growth. The determination of xylem cell identity from vascular stem cells is therefore crucial for the formation of secondary xylem. Formation of the secondary xylem initiates with a vascular stem cell whose cell lineages divide and differentiate in a largely unknown spatio-temporal manner. Impaired or delayed secondary xylem formation has destructive effects on radial vascular patterning and plant growth. Understanding the spatio-temporal pattern of the regulatory networks behind secondary xylem formation is therefore crucial to improve xylem formation, plant growth and wood production. In this study, I report two novel roles of strigolactone (SL) signaling in vascular development in Arabidopsis thaliana: SL signaling suppresses secondary vessel formation at xylem phase I and maintains the radial hypocotyl patterning at xylem phase II. During xylem phase I, SL signaling is highly associated with most of the differentiated tissues as revealed by promoter activity analysis. In comparison, I detected a relatively low SL signaling level in developing vessel elements. A prominent increase in secondary vessel formation was detected in the SL signaling mutant dwarf14 (d14) based on both single nucleus RNA-sequencing (snRNA-seq) and histological analysis, while deficiency in SUPPRESSOR OF MAX2 1-LIKE6 (SMXL6), SMXL7 and SMXL8 gene activities resulted in reduced secondary vessel formation. SMXL7 was sufficient to promote secondary vessel formation, which I concluded based on a comparable enhancement of secondary vessel formation in d14 mutants and in lines expressing a stabilized SMXL7 (SMXL7d53) protein. Vessel size and number were reduced when auxin signaling was repressed in the PHLOEM INTERCALATED WITH XYLEM (PXY) expression domain in d14 mutants. This suggested that SL and auxin signaling play interconnected roles in secondary vessel formation. During phase II, I observed a disrupted radial hypocotyl patterning in d14 mutants accompanied by an altered auxin response along the radial sequence of hypocotyl tissues as revealed by a DR5revV2:EYFP-ER reporter. Importantly, the disrupted radial hypocotyl pattern in d14 mutants was completely recovered to a wild type-like pattern either by repressing auxin signaling in the SMXL5 expression domain or under MONOPTEROS (MP) deficiency conditions. This demonstrated that SL signaling is crucial for maintaining the radial hypocotyl patterning via modulating the radial auxin response pattern which is mainly mediated by MP.