A critical role of sterols in embryonic patterning and meristem programming revealed by the fackel mutants of Arabidopsis thaliana
- Jyan-Chyun Jang1,6,
- Shozo Fujioka2,
- Masao Tasaka3,
- Hideharu Seto2,
- Suguru Takatsuto4,
- Akira Ishii3,
- Mitsuhiro Aida3,
- Shigeo Yoshida2, and
- Jen Sheen5
- 1Department of Horticulture and Crop Science, The Ohio State University, Columbus, Ohio 43210 USA; 2The Institute of Physical and Chemical Research (RIKEN), Wako-shi, Saitama 351-0198, Japan; 3Graduate School of Bioscience, NAIST (Nara Institute Of Science and Technology), Ikoma Nara 630-0101, Japan; 4Department of Chemistry, Joetsu University of Education, Joetsu-shi, Niigata 943-8512, Japan; 5Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114 USA
Abstract
Here we report a novel Arabidopsis dwarf mutant,fackel-J79, whose adult morphology resembles that of brassinosteroid-deficient mutants but also displays distorted embryos, supernumerary cotyledons, multiple shoot meristems, and stunted roots. We cloned the FACKEL gene and found that it encodes a protein with sequence similarity to both the human sterol reductase family and yeast C-14 sterol reductase and is preferentially expressed in actively growing cells. Biochemical analysis indicates that the fk-J79mutation results in deficient C-14 sterol reductase activity, abnormal sterol composition, and reduction of brassinosteroids (BRs). Unlike other BR-deficient mutants, the defect of hypocotyl elongation infk-J79 cannot be corrected by exogenous BRs. The unique phenotypes and sterol composition in fk-J79 indicate crucial roles of sterol regulation and signaling in cell division and cell expansion in embryonic and post-embryonic development in plants.
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Footnotes
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↵6 Corresponding author.
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E-MAIL jang.40{at}osu.edu; FAX (614) 292-7162.
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- Received February 18, 2000.
- Accepted April 18, 2000.
- Cold Spring Harbor Laboratory Press
