4.5 Article

Genetic fine mapping and candidate gene analysis of the Gossypium hirsutum Ligon lintless-1 (Li1) mutant on chromosome 22(D)

期刊

MOLECULAR GENETICS AND GENOMICS
卷 290, 期 6, 页码 2199-2211

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s00438-015-1070-2

关键词

Cotton; Fiber; Ligon lintless-1; Genetic mapping; Single-strand conformation polymorphism (SSCP) marker

资金

  1. National High Technology Research and Development Program of China (863 Program) [2011AA100202]
  2. National Natural Science Foundation of China [31200909, 31301372]
  3. State Key Laboratory of Cotton Biology Open Fund [CB2014A06]

向作者/读者索取更多资源

Ligon lintless-1 (Li1) is a Gossypium hirsutum mutant that is controlled by a dominant gene that arrests the development of cotton fiber after anthesis. Two F-2 mapping populations were developed from mutant (Li1 x H7124) F-1 plants in 2012 and 2013; each was composed of 142 and 1024 plants, respectively. Using these populations, Li1 was mapped to a 0.3-cM region in which nine single-strand conformation polymorphism markers co-segregated with the Li1 locus. In the published G. raimondii genome, these markers were mapped to a region of about 1.2 Mb (the Li1 region) and were separated by markers that flanked the Li1 locus in the genetic map, dividing the Li1 region into three segments. Thirty-six genes were annotated by the gene prediction software FGENESH (Softberry) in the Li1 region. Twelve genes were candidates of Li1, while the remaining 24 genes were identified as transposable elements, DNA/RNA polymerase superfamily or unknown function genes. Among the 12 candidate genes, those encoding ribosomal protein s10, actin protein, ATP synthase, and beta-tubulin 5 were the most-promising candidates of the Li1 mutant because the function of these genes is closely related to fiber development. High-throughput RNA sequencing and quantitative PCR revealed that these candidate genes had obvious differential gene expression between mutant and wild-type plants at the fiber elongation stage, strengthening the inference that they could be the most likely candidate gene of the Li1 mutant phenotype.

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