Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Genetic linkage map and QTL analysis of partial resistance to black stem in sunflower (Helianthus annuus L.)

Genetic linkage map and QTL analysis of partial resistance to black stem in sunflower (Helianthus... Black stem, caused by Phoma macdonaldii, is one of the most important diseases of sunflower in the world. Quantitative trait loci (QTLs) implicated in partial resistance to three isolates of P. macdonaldii including MA6, MP6 and MP10 were investigated using F2/F3 population from the cross between sunflower resistant mutant line ‘M6-54-1’ and susceptible inbred line ‘ENSAT-B4’. A genetic linkage map was constructed with 88 amplified fragment length polymorphism (AFLP) and 44 simple sequence repeat (SSR) markers using 101 F2 individuals. The map comprises 17 linkage groups (LGs) with an overall length of 1,490 cM and mean density of one marker per 12.44 cM. Parental lines and their 101 F3 families were evaluated for their resistance to P. macdonalii isolates in controlled conditions in a randomized complete block design with three replications. High genetic variability and transgressive segregation were observed among F3 families for partial resistance to all of three P. macdonaldii isolates. Composite interval mapping analysis revealed 14 putative QTLs, localized on seven linkage groups, with phenotypic variance ranging from 4 to 42 %. The QTL bsrMP6.8.1 was detected as non isolate-specific QTL and the rest of them were ‘isolate-specific’ QTLs. The major QTL on LG8 which was involved in partial resistance to three isolates could be good candidate to introduce resistance to three P. macdonaldii isolates into elite sunflower breeding lines via marker assisted breeding program. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Australasian Plant Pathology Springer Journals

Genetic linkage map and QTL analysis of partial resistance to black stem in sunflower (Helianthus annuus L.)

Loading next page...
 
/lp/springer-journals/genetic-linkage-map-and-qtl-analysis-of-partial-resistance-to-black-M6nK2qDaOY

References (49)

Publisher
Springer Journals
Copyright
Copyright © 2013 by Australasian Plant Pathology Society Inc.
Subject
Life Sciences; Plant Pathology; Plant Sciences; Agriculture; Entomology; Ecology
ISSN
0815-3191
eISSN
1448-6032
DOI
10.1007/s13313-013-0265-4
Publisher site
See Article on Publisher Site

Abstract

Black stem, caused by Phoma macdonaldii, is one of the most important diseases of sunflower in the world. Quantitative trait loci (QTLs) implicated in partial resistance to three isolates of P. macdonaldii including MA6, MP6 and MP10 were investigated using F2/F3 population from the cross between sunflower resistant mutant line ‘M6-54-1’ and susceptible inbred line ‘ENSAT-B4’. A genetic linkage map was constructed with 88 amplified fragment length polymorphism (AFLP) and 44 simple sequence repeat (SSR) markers using 101 F2 individuals. The map comprises 17 linkage groups (LGs) with an overall length of 1,490 cM and mean density of one marker per 12.44 cM. Parental lines and their 101 F3 families were evaluated for their resistance to P. macdonalii isolates in controlled conditions in a randomized complete block design with three replications. High genetic variability and transgressive segregation were observed among F3 families for partial resistance to all of three P. macdonaldii isolates. Composite interval mapping analysis revealed 14 putative QTLs, localized on seven linkage groups, with phenotypic variance ranging from 4 to 42 %. The QTL bsrMP6.8.1 was detected as non isolate-specific QTL and the rest of them were ‘isolate-specific’ QTLs. The major QTL on LG8 which was involved in partial resistance to three isolates could be good candidate to introduce resistance to three P. macdonaldii isolates into elite sunflower breeding lines via marker assisted breeding program.

Journal

Australasian Plant PathologySpringer Journals

Published: Dec 30, 2013

There are no references for this article.