Molecular Genetics and Genomics

, Volume 283, Issue 4, pp 305–315

Gain of deleterious function causes an autoimmune response and Bateson–Dobzhansky–Muller incompatibility in rice

  • Eiji Yamamoto
  • Tomonori Takashi
  • Yoichi Morinaka
  • Shaoyang Lin
  • Jianzhong Wu
  • Takashi Matsumoto
  • Hidemi Kitano
  • Makoto Matsuoka
  • Motoyuki Ashikari
Original Paper

DOI: 10.1007/s00438-010-0514-y

Cite this article as:
Yamamoto, E., Takashi, T., Morinaka, Y. et al. Mol Genet Genomics (2010) 283: 305. doi:10.1007/s00438-010-0514-y

Abstract

Reproductive isolation plays an important role in speciation as it restricts gene flow and accelerates genetic divergence between formerly interbreeding population. In rice, hybrid breakdown is a common reproductive isolation observed in both intra and inter-specific crosses. It is a type of post-zygotic reproductive isolation in which sterility and weakness are manifested in the F2 and later generations. In this study, the physiological and molecular basis of hybrid breakdown caused by two recessive genes, hbd2 and hbd3, in a cross between japonica variety, Koshihikari, and indica variety, Habataki, were investigated. Fine mapping of hbd2 resulted in the identification of the causal gene as casein kinase I (CKI1). Further analysis revealed that hbd2-CKI1 allele gains its deleterious function that causes the weakness phenotype by a change of one amino acid. As for the other gene, hbd3 was mapped to the NBS-LRR gene cluster region. It is the most common class of R-gene that triggers the immune signal in response to pathogen attack. Expression analysis of pathogen response marker genes suggested that weakness phenotype in this hybrid breakdown can be attributed to an autoimmune response. So far, this is the first evidence linking autoimmune response to post-zygotic isolation in rice. This finding provides a new insight in understanding the molecular and evolutionary mechanisms establishing post-zygotic isolation in plants.

Keywords

RiceReproductive isolationBDM incompatibilityAutoimmune responseWeakness phenotype

Supplementary material

438_2010_514_MOESM1_ESM.xls (32 kb)
Supplementary Table 1 (XLS 32 kb)
438_2010_514_MOESM2_ESM.xls (31 kb)
Supplementary Table 2 (XLS 31 kb)

Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  • Eiji Yamamoto
    • 1
  • Tomonori Takashi
    • 2
  • Yoichi Morinaka
    • 2
  • Shaoyang Lin
    • 2
  • Jianzhong Wu
    • 3
  • Takashi Matsumoto
    • 3
  • Hidemi Kitano
    • 1
  • Makoto Matsuoka
    • 1
  • Motoyuki Ashikari
    • 1
  1. 1.Bioscience and Biotechnology CenterNagoya UniversityNagoyaJapan
  2. 2.Honda Research Institute JapanKisarazuJapan
  3. 3.National Institute of Agrobiological ResourcesTsukubaJapan