The inheritance of anther extrusion in hexaploid wheat and its relationship to Fusarium head blight resistance and deoxynivalenol content uri icon

abstract

  • Anther extrusion (AE) has been suggested as one of the resistance mechanisms to Fusarium head blight (FHB) in wheat, but not well investigated. The objectives of this study were to assess AE in the double haploid population _Arina_ ? _NK93604_, evaluate its relationship both with FHB and deoxynivalenol (DON) accumulation, and map quantitative trait loci (QTLs). AE was studied in 2005)2007 and its relationship to FHB and DON content was analysed with data from Fusarium culmorum inoculations in 2001-2003 and with Fusarium graminearum in 2007. AE showed continuous distribution, transgressive segregation, minimal genotype - year interactions and was highly heritable (H2 = 0.91). Mean AE showed highly significant negative correlations both with FHB (r = )0.53 to )0.69, P = 0.0001) and DON (r = )0.39 to )0.46, P = 0.0001). Composite interval mapping identified 4 QTLs for mean AE over 2 years that explained 53.6% of the total phenotypic variation. The phenotypic variance explained by the QTLs on chromosomes 1AL, 1BL, 4DL and 6AS varied from 7.4% to 18.3%. This is the first report describing QTLs for AE and to look systematically for association of AE with FHB and DON
  • P>Anther extrusion (AE) has been suggested as one of the resistance mechanisms to Fusarium head blight (FHB) in wheat, but not well investigated. The objectives of this study were to assess AE in the double haploid population 'Arina' x 'NK93604', evaluate its relationship both with FHB and deoxynivalenol (DON) accumulation, and map quantitative trait loci (QTLs). AE was studied in 2005-2007 and its relationship to FHB and DON content was analysed with data from Fusarium culmorum inoculations in 2001-2003 and with Fusarium graminearum in 2007. AE showed continuous distribution, transgressive segregation, minimal genotype x year interactions and was highly heritable (H2 = 0.91). Mean AE showed highly significant negative correlations both with FHB (r = -0.53 to -0.69, P = 0.0001) and DON (r = -0.39 to -0.46, P = 0.0001). Composite interval mapping identified 4 QTLs for mean AE over 2 years that explained 53.6% of the total phenotypic variation. The phenotypic variance explained by the QTLs on chromosomes 1AL, 1BL, 4DL and 6AS varied from 7.4% to 18.3%. This is the first report describing QTLs for AE and to look systematically for association of AE with FHB and DON.

publication date

  • 2010
  • 2010
  • 2010