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A new SNP haplotype associated with blue disease resistance gene in cotton (Gossypium hirsutum L.)

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Abstract

Resistance to cotton blue disease (CBD) was evaluated in 364 F2.3 families of three populations derived from resistant variety ‘Delta Opal’. The CBD resistance in ‘Delta Opal’ was controlled by one single dominant gene designated Cbd. Two simple sequence repeat (SSR) markers were identified as linked to Cbd by bulked segregant analysis. Cbd resides at the telomere region of chromosome 10. SSR marker DC20027 was 0.75 cM away from Cbd. DC20027 marker fragments amplified from 3 diploid species and 13 cotton varieties whose CBD resistance was known were cloned and sequenced. One single nucleotide polymorphism (SNP) was identified at the 136th position by sequence alignment analysis. Screening SNP markers previously mapped on chromosome 10 identified an additional 3 SNP markers that were associated with Cbd. A strong association between a haplotype based on four SNP markers and Cbd was developed. This demonstrates one of the first examples in cotton where SNP markers were used to effectively tag a trait enabling marker-assisted selection for high levels of CBD resistance in breeding programs.

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Acknowledgment

We greatly thank two anonymous reviewers who made excellent suggestions for revising the manuscript.

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Authors and Affiliations

  1. Cotton Fiber Bioscience Research Unit, USDA-ARS-SRRC, 1100 Robert E. Lee Blvd., New Orleans, LA, 70124, USA

    David D. Fang

  2. Monsanto Company, 800 North Lindbergh Blvd., St. Louis, MO, 63167, USA

    Jinhua Xiao & Roy G. Cantrell

  3. Monsanto Company, Av. Alexandre Ribeiro Guimaraes #620, Uberlandia, Minas Gerais, 384085, Brazil

    Paulo C. Canci

Authors
  1. David D. Fang
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  2. Jinhua Xiao
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  3. Paulo C. Canci
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  4. Roy G. Cantrell
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Corresponding author

Correspondence to Roy G. Cantrell.

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Communicated by I. Mackay.

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Fang, D.D., Xiao, J., Canci, P.C. et al. A new SNP haplotype associated with blue disease resistance gene in cotton (Gossypium hirsutum L.). Theor Appl Genet 120, 943–953 (2010). https://doi.org/10.1007/s00122-009-1223-y

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  • DOI: https://doi.org/10.1007/s00122-009-1223-y

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