Brassinosteroid Deficiency Due to Truncated Steroid 5a-Reductase Causes Dwarfism in the lk Mutant of Pea
journal contribution
posted on 2023-06-14, 09:43authored byNomura, T, Jager, CE, Kitasaka, Y, Takeuchi, K, Fukami, M, Yoneyama, K, Matsushita, Y, Nyunoya, H, Takatsuto, S, Fujioka, S, Smith, JJ, Kerckhoffs, LHJ, James ReidJames Reid, Yokota, T
The endogenous brassinosteroids in the dwarf mutant lk of pea (Pisum sativum) were quantified by gas chromatographyselected ion monitoring. The levels of castasterone, 6-deoxocastasterone, and 6-deoxotyphasterol in lk shoots were reduced 4-, 70-, and 6-fold, respectively, compared with those of the wild type. The fact that the application of brassinolide restored the growth of the mutant indicated that the dwarf mutant lk is brassinosteroid deficient. Gas chromatography-selected ion monitoring analysis of the endogenous sterols in lk shoots revealed that the levels of campestanol and sitostanol were reduced 160- and 10-fold, respectively, compared with those of wild-type plants. These data, along with metabolic studies, showed that the lk mutant has a defect in the conversion of campest-4-en-3-one to 5a-campestan-3-one, which is a key hydrogenation step in the synthesis of campestanol from campesterol. This defect is the same as that found in the Arabidopsis det2 mutant and the Ipomoea nil kbt mutant. The pea gene homologous to the DET2 gene, PsDET2, was cloned, and it was found that the lk mutation would result in a putative truncated PsDET2 protein. Thus it was concluded that the short stature of the lk mutant is due to a defect in the steroidal 5a-reductase gene. This defect was also observed in the callus induced from the lk mutant. Biosynthetic pathways involved in the conversion of campesterol to campestanol are discussed in detail.
History
Publication title
Plant Physiology
Volume
135
Pagination
2220-2229
ISSN
0032-0889
Publication status
Published
Rights statement
Copyright Copyright 2004 American Society of Plant Biologists