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A novel Arabidopsis gene TONSOKU is required for proper cell arrangement in root and shoot apical meristems
Author(s) -
Suzuki Takamasa,
Inagaki Soichi,
Nakajima Sakiko,
Akashi Takafumi,
Ohto Masaaki,
Kobayashi Masatomo,
Seki Motoaki,
Shinozaki Kazuo,
Kato Tomohiko,
Tabata Satoshi,
Nakamura Kenzo,
Morikami Atsushi
Publication year - 2004
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2004.02074.x
Subject(s) - meristem , mutant , biology , cell division , arabidopsis , cytokinesis , genetics , gene , microbiology and biotechnology , arabidopsis thaliana , cell
Summary Root apical meristem (RAM) and shoot apical meristem (SAM) are vital for the correct development of the plant. The direction, frequency, and timing of cell division must be tightly controlled in meristems. Here, we isolated new Arabidopsis mutants with shorter roots and fasciated stems. In the tonsoku ( tsk ) mutant, disorganized RAM and SAM formation resulted from the frequent loss of proper alignment of the cell division plane. Irregular cell division also occurred in the tsk embryo, and the size of cells in meristems and embryo in tsk mutant was larger than in the wild type. In the enlarged SAM of the tsk mutant, multiple centers of cells expressing WUSCHEL ( WUS ) were observed. In addition, expression of SCARECROW ( SCR ) in the quiescent center (QC) disappeared in the disorganized RAM of tsk mutant. These results suggest that disorganized cell arrangements in the tsk mutants result in disturbed positional information required for the determination of cell identity. The TSK gene was found to encode a protein with 1311 amino acids that possesses two types of protein–protein interaction motif, leucine–glycine–asparagine (LGN) repeats and leucine‐rich repeats (LRRs). LGN repeats are present in animal proteins involved in asymmetric cell division, suggesting the possible involvement of TSK in cytokinesis. On the other hand, the localization of the TSK–GFP (green fluorescent protein) fusion protein in nuclei of tobacco BY‐2 cells and phenotypic similarity of tsk mutants to other fasciated mutants suggest that the tsk mutation may cause disorganized cell arrangements through defects in genome maintenance.