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BIN4, a Novel Component of the Plant DNA Topoisomerase VI Complex, Is Required for Endoreduplication in Arabidopsis^[W],[OA]

^a Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, United Kingdom
^b Department of Biological Chemistry, John Innes Centre, Norwich NR4 7UH, United Kingdom
^c RIKEN Plant Science Center, Tsurumi, Yokohama, Kanagawa 230-0045, Japan
^d Centre for Plant Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom
^e Section of Cell and Developmental Biology, University of California at San Diego, La Jolla, California 92093-0116
^f Howard Hughes Medical Institute and Plant Biology Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037
^g Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan
^h National Institute for Basic Biology, Myodaiji-cho, Okazaki 444-8585, Japan
ⁱ Department of Biological Sciences, Kanagawa University, Hiratsuka, Kanagawa 259-1293, Japan

¹ Address correspondence to sugimoto{at}psc.riken.jp.

How plant organs grow to reach their final size is an important but largely unanswered question. Here, we describe an Arabidopsis thaliana mutant, brassinosteroid-insensitive4 (bin4), in which the growth of various organs is dramatically reduced. Small organ size in bin4 is primarily caused by reduced cell expansion associated with defects in increasing ploidy by endoreduplication. Raising nuclear DNA content in bin4 by colchicine-induced polyploidization partially rescues the cell and organ size phenotype, indicating that BIN4 is directly and specifically required for endoreduplication rather than for subsequent cell expansion. BIN4 encodes a plant-specific, DNA binding protein that acts as a component of the plant DNA topoisomerase VI complex. Loss of BIN4 triggers an ATM- and ATR-dependent DNA damage response in postmitotic cells, and this response coincides with the upregulation of the cyclin B1;1 gene in the same cell types, suggesting a functional link between DNA damage response and endocycle control.