Transcription factor NTL9 negatively regulates Arabidopsis vascular cambium development during stem secondary growth

Abstract In plant stems, secondary vascular development is established through the differentiation of cylindrical vascular cambium, producing secondary xylem (wood) and phloem (bast), which have economic importance. However, there is a dearth of knowledge on the genetic mechanism underlying this pro...

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Published inPlant physiology (Bethesda) Vol. 190; no. 3; pp. 1731 - 1746
Main Authors Sugimoto, Hiroki, Tanaka, Tomoko, Muramoto, Nobuhiko, Kitagawa-Yogo, Ritsuko, Mitsukawa, Norihiro
Format Journal Article
LanguageEnglish
Published Oxford University Press 27.10.2022
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Summary:Abstract In plant stems, secondary vascular development is established through the differentiation of cylindrical vascular cambium, producing secondary xylem (wood) and phloem (bast), which have economic importance. However, there is a dearth of knowledge on the genetic mechanism underlying this process. NAC with Transmembrane Motif 1-like transcription factor 9 (NTL9) plays a central role in abiotic and immune signaling responses. Here, we investigated the role of NTL9 in vascular cambium development in Arabidopsis (Arabidopsis thaliana) inflorescence stems by identifying and characterizing an Arabidopsis phloem circular-timing (pct) mutant. The pct mutant exhibited enhanced vascular cambium formation following secondary phloem production. In the pct mutant, although normal organization in vascular bundles was maintained, vascular cambium differentiation occurred at an early stage of stem development, which was associated with increased expression of cambium-/phloem-related genes and enhanced cambium activity. The pct mutant stem phenotype was caused by a recessive frameshift mutation that disrupts the transmembrane (TM) domain of NTL9. Our results indicate that NTL9 functions as a negative regulator of cambial activity and has a suppressive role in developmental transition to the secondary growth phase in stem vasculature, which is necessary for its precise TM domain-mediated regulation.
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These authors contributed equally to this work (H.S. and T.T.)
Senior author
ISSN:0032-0889
1532-2548
DOI:10.1093/plphys/kiac368