MSH1-induced non-genetic variation provides a source of phenotypic diversity in Sorghum bicolor

PLoS One. 2014 Oct 27;9(10):e108407. doi: 10.1371/journal.pone.0108407. eCollection 2014.


MutS Homolog 1 (MSH1) encodes a plant-specific protein that functions in mitochondria and chloroplasts. We showed previously that disruption or suppression of the MSH1 gene results in a process of developmental reprogramming that is heritable and non-genetic in subsequent generations. In Arabidopsis, this developmental reprogramming process is accompanied by striking changes in gene expression of organellar and stress response genes. This developmentally reprogrammed state, when used in crossing, results in a range of variation for plant growth potential. Here we investigate the implications of MSH1 modulation in a crop species. We found that MSH1-mediated phenotypic variation in Sorghum bicolor is heritable and potentially valuable for crop breeding. We observed phenotypic variation for grain yield, plant height, flowering time, panicle architecture, and above-ground biomass. Focusing on grain yield and plant height, we found some lines that appeared to respond to selection. Based on amenability of this system to implementation in a range of crops, and the scope of phenotypic variation that is derived, our results suggest that MSH1 suppression provides a novel approach for breeding in crops.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Breeding
  • Chloroplasts / genetics
  • Chloroplasts / metabolism
  • Crops, Agricultural
  • Environment
  • Gene-Environment Interaction
  • Genetic Association Studies
  • Genetic Variation*
  • Microsatellite Repeats
  • MutS DNA Mismatch-Binding Protein / genetics*
  • MutS DNA Mismatch-Binding Protein / metabolism
  • Phenotype*
  • Plants, Genetically Modified
  • Polymorphism, Single Nucleotide
  • Quantitative Trait, Heritable
  • Sorghum


  • MutS DNA Mismatch-Binding Protein

Grant support

This work was supported by grants from the Bill & Melinda Gates Foundation (OPP1059119, and the National Science Foundation (IOS-1126935, The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.