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Fitness costs of R-gene-mediated resistance in Arabidopsis thaliana

Author

Listed:
  • D. Tian

    (University of Chicago)

  • M. B. Traw

    (University of Chicago)

  • J. Q. Chen

    (Nanjing University)

  • M. Kreitman

    (University of Chicago)

  • J. Bergelson

    (University of Chicago)

Abstract

Resistance genes (R-genes) act as an immune system in plants by recognizing pathogens and inducing defensive pathways. Many R-gene loci are present in plant genomes, presumably reflecting the need to maintain a large repertoire of resistance alleles. These loci also often segregate for resistance and susceptibility alleles that natural selection has maintained as polymorphisms within a species for millions of years1,2,3,4,5. Given the obvious advantage to an individual of being disease resistant, what prevents these resistance alleles from being driven to fixation by natural selection? A cost of resistance6 is one potential explanation; most models require a lower fitness of resistant individuals in the absence of pathogens for long-term persistence of susceptibility alleles7. Here we test for the presence of a cost of resistance at the RPM1 locus of Arabidopsis thaliana. Results of a field experiment comparing the fitness of isogenic strains that differ in the presence or absence of RPM1 and its natural promoter reveal a large cost of RPM1, providing the first evidence that costs contribute to the maintenance of an ancient R-gene polymorphism.

Suggested Citation

  • D. Tian & M. B. Traw & J. Q. Chen & M. Kreitman & J. Bergelson, 2003. "Fitness costs of R-gene-mediated resistance in Arabidopsis thaliana," Nature, Nature, vol. 423(6935), pages 74-77, May.
  • Handle: RePEc:nat:nature:v:423:y:2003:i:6935:d:10.1038_nature01588
    DOI: 10.1038/nature01588
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    Cited by:

    1. Aleksandra Noweiska & Roksana Bobrowska & MichaƂ Tomasz Kwiatek, 2022. "Structural Polymorphisms of Chromosome 3A m Containing Lr63 Leaf Rust Resistance Loci Reflect the Geographical Distribution of Triticum monococcum L. and Related Diploid Wheats," Agriculture, MDPI, vol. 12(7), pages 1-11, July.
    2. DeAngelis, Donald L. & Koslow, Jennifer M. & Jiang, Jiang & Ruan, Shigui, 2008. "Host mating system and the spread of a disease-resistant allele in a population," Theoretical Population Biology, Elsevier, vol. 74(2), pages 191-198.
    3. Shen Huang & Chunli Wang & Zixuan Ding & Yaqian Zhao & Jing Dai & Jia Li & Haining Huang & Tongkai Wang & Min Zhu & Mingfeng Feng & Yinghua Ji & Zhongkai Zhang & Xiaorong Tao, 2024. "A plant NLR receptor employs ABA central regulator PP2C-SnRK2 to activate antiviral immunity," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    4. Joo Hyun Im & Brian P Lazzaro, 2018. "Population genetic analysis of autophagy and phagocytosis genes in Drosophila melanogaster and D. simulans," PLOS ONE, Public Library of Science, vol. 13(10), pages 1-17, October.
    5. Andy Fenton & Michael A Brockhurst, 2007. "Epistatic Interactions Alter Dynamics of Multilocus Gene-for-Gene Coevolution," PLOS ONE, Public Library of Science, vol. 2(11), pages 1-6, November.
    6. Yuying Li & Qiong Wang & Huimin Jia & Kazuya Ishikawa & Ken-ichi Kosami & Takahiro Ueba & Atsumi Tsujimoto & Miki Yamanaka & Yasuyuki Yabumoto & Daisuke Miki & Eriko Sasaki & Yoichiro Fukao & Masayuki, 2024. "An NLR paralog Pit2 generated from tandem duplication of Pit1 fine-tunes Pit1 localization and function," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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