4.7 Article

Genome-wide analysis of BES1 genes in Gossypium revealed their evolutionary conserved roles in brassinosteroid signaling

Journal

SCIENCE CHINA-LIFE SCIENCES
Volume 61, Issue 12, Pages 1566-1582

Publisher

SCIENCE PRESS
DOI: 10.1007/s11427-018-9412-x

Keywords

G. hirsutum; brassinosteroids; BES1; phylogenetic; collinearity; duplication; hormones; curled leaves; hypocotyl

Categories

Funding

  1. National Natural Science Foundation of China [31501345]
  2. Young Elite Scientist Sponsorship Program by CAST (China Association for Science and Technology)

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Brassinosteroids (BRs), which are essential phytohormones for plant growth and development, are important for cotton fiber development. Additionally, BES1 transcription factors are critical for BR signal transduction. However, cotton BES1 family genes have not been comprehensively characterized. In this study, we identified 11 BES1 genes in G. arboreum, 11 in G. raimondii, 16 in G. barbadense, and 22 in G. hirsutum. The BES1 sequences were significantly conserved in the Arabidopsis thaliana, rice, and upland cotton genomes. A total of 94 BES1 genes from 10 different plant species were divided into three clades according to the neighbor-joining and minimum-evolution methods. Moreover, the exon/intron patterns and motif distributions were highly conserved among the A. thaliana and cotton BES1 genes. The collinearity among the orthologs from the At and Dt subgenomes was estimated. Segmental duplications in the At and Dt subgenomes were primarily responsible for the expansion of the cotton BES1 gene family. Of the GhBES1 genes, GhBES1.4_At/Dt exhibited BL-induced expression and was predominantly expressed in fibers. Furthermore, Col-0/mGhBES1.4_At plants produced curled leaves with long and bent petioles. These transgenic plants also exhibited decreased hypocotyl sensitivity to brassinazole and constitutive BR induced/repressed gene expression patterns. The constitutive BR responses of the plants overexpressing mGhBES1.4_At were similar to those of the bes1-D mutant.

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