Full text
| |
| Author(s): |
Maria Teresa Gomes Lopes
Total Authors: 1
|
| Document type: | Doctoral Thesis |
| Press: | Piracicaba. |
| Institution: | Universidade de São Paulo (USP). Escola Superior de Agricultura Luiz de Queiroz (ESALA/BC) |
| Defense date: | 2003-03-20 |
| Advisor: | Luis Eduardo Aranha Camargo |
| Abstract | |
The objective of the present work was to estimate the mode of inheritance of resistance to Phaeosphaeria leaf spot of maize through generation mean analysis and to map quantitative resistance loci (QRL) with molecular markers. The analysis of generations was carried out for two populations derived from crossings of two resistant lines (DAS72 and DAS95) with a susceptible one (DAS21). Disease severity was evaluated 30 days after flowering using a diagrammatic scale. The mean disease severity of the paternal, F1, F2, BCP1 and BCP2 generations were analyzed according to the model of Mather and Jinks (1971). Results evidenced the importance of additive genetic effects compared to the dominant ones in both populations. The genetic variation due to additive effects accounted for 73% and 74% of the total genetic variance in each population. Resistance to Phaeosphaeria leaf spot was highly inheritable in the broad sense (71% and 63%, respectively for the populations originated from DAS95 x DAS21 and DAS72 x DAS21) and oligogenic. Mapping of QRLs was accomplished based on the analysis of 118 F3 families derived from DAS95 x DAS21, evaluated in two field trials with three replications each. Disease severity was evaluated at the flowering time and 15 and 30 days after. These evaluations were used to calculate the AUDPC (area under the curve of disease progress) for each family. Linkage analyses between markers and QRLs were made using multiple linear regression (MLR) and composite interval mapping (CIM). The proportion of the phenotypic variation in resistance due to the association of QRLs with markers for each evaluation and AUDPC of the two experiments as well as for the mean values of both experiments varied from 33% to 45%, according to MLR analysis. Considering the three individual evaluations and AUDPC, 10 markers were found linked to QRLs in the first experiment, 9 in the second and 9 in the joint analysis in six different chromosomes. A QRL was identified linked to a marker not allocated to any chromosome. Evidences of QRLs x environment interactions emphasized the importance of evaluating populations in different environments. The results of CIM analysis identified QRLs in 10 intervals, 2 in chromosome 1, 2 in chromosome 2, 3 in chromosome 4, 1 in chromosome 5, 1 in chromosome 6 and 1 in chromosome 9. Resistance alleles were identified in both genitors, although alleles from the resistant genitor contributed most to resistance. (AU) | |