Ideal type 1 is caused by a point mutation in the α-tubulin gene that affects microtubule arrangement in soybean
Bohong Su,
Yong Guo,
Zhongfeng Li,
Huawei Gao,
Zhongyan Wei,
Lijuan Qiu
Affiliations
Bohong Su
College of Agriculture, Northeast Agricultural University, Harbin 150030, Heilongjiang, China; National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing 100081, China
Yong Guo
National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing 100081, China
Zhongfeng Li
College of Agronomy, Henan Agricultural University, Zhengzhou 450002, Henan, China
Huawei Gao
National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing 100081, China
Zhongyan Wei
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Key Laboratory of Biotechnology in Plant Protection of MARA of China and Zhejiang Province, Institute of Plant Virology, Ningbo University, Ningbo 315211, Zhejiang, China
Lijuan Qiu
College of Agriculture, Northeast Agricultural University, Harbin 150030, Heilongjiang, China; National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing 100081, China; Corresponding author.
Plant architecture is a target of crop improvement. The soybean mutant ideal type 1 (it1) displays a pleiotropic phenotype characterized by compact plant architecture, reduced plant height, shortened petioles, wrinkled leaves, and indented seeds. Genetic analysis revealed that the pleiotropic phenotype was controlled by an incomplete dominant gene. We characterized the cellular phenotypes of it1 and positionally cloned the it1 locus. Detailed morphogenetic analysis of the it1 mutant revealed an excess of xylem cells and expanded phloem, and polygonal pavement cells. Positional cloning showed that the phenotype was caused by a G-to-A mutation in the second exon of the α-tubulin gene (Glyma.05G157300). The mutation altered microtubule arrangement in pavement cells, changing their morphology. Overexpression of Gmit1 resulted in an it1-like phenotype and polygonal pavement cells and microtubules of overexpressors were parallel or slightly inclined. Five suppressor mutants able to suppress the phenotype of it1 were obtained by EMS mutagenesis in the it1 background. All these mutants carried an additional mutation in the it1 gene. These results suggest that the pleiotropic phenotype of it1 is caused by the mutation in the α-tubulin gene.
