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First published online 3 July 2008
doi: 10.1242/dev.019349

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ACAULIS5 controls Arabidopsis xylem specification through the prevention of premature cell death

Luis Muñiz^1,*,, Eugenio G. Minguet^2,*, Sunil Kumar Singh^1,*, Edouard Pesquet^1,, Francisco Vera-Sirera², Charleen L. Moreau-Courtois¹, Juan Carbonell², Miguel A. Blázquez^2, and Hannele Tuominen¹

¹ Umeå Plant Science Centre, Department of Plant Physiology, Umeå University, 90187 Umeå, Sweden.
² Instituto de Biología Molecular y Celular de Plantas (CSIC-UPV), Universidad Politécnica de Valencia, Avda de los Naranjos s/n, 46022 Valencia, Spain.

Author for correspondence (e-mail: mblazquez{at}ibmcp.upv.es)

Accepted 26 May 2008

Cell size and secondary cell wall patterning are crucial for the proper functioning of xylem vessel elements in the vascular tissues of plants. Through detailed anatomical characterization of Arabidopsis thaliana hypocotyls, we observed that mutations in the putative spermine biosynthetic gene ACL5 severely affected xylem specification: the xylem vessel elements of the acl5 mutant were small and mainly of the spiral type, and the normally predominant pitted vessels as well as the xylem fibers were completely missing. The cell-specific expression of ACL5 in the early developing vessel elements, as detected by in situ hybridization and reporter gene analyses, suggested that the observed xylem vessel defects were caused directly by the acl5 mutation. Exogenous spermine prolonged xylem element differentiation and stimulated cell expansion and cell wall elaboration in xylogenic cell cultures of Zinnia elegans, suggesting that ACL5 prevents premature death of the developing vessel elements to allow complete expansion and secondary cell wall patterning. This was further supported by our observations that the vessel elements of acl5 seemed to initiate the cell death program too early and that the xylem defects associated with acl5 could be largely phenocopied by induction of premature, diphtheria toxin-mediated cell death in the ACL5-expressing vessel elements. We therefore provide, for the first time, mechanistic evidence for the function of ACL5 in xylem specification through its action on the duration of xylem element differentiation.

Key words: ACL5, Arabidopsis, Cell death, Secondary cell wall, Tracheary element, Xylem specification

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