scholarly journals A Fine mapping quantitative trait loci that underlie resistance to soybean sudden death syndrome using NILs and SNPs.

2018 ◽  
pp. 583-591
Author(s):  
Yi Chen Lee ◽  
M Javed Iqbal ◽  
Victor N Njiti ◽  
Stella Kantartzi ◽  
David A. Lightfoot

Soybean (Glycine max (L.) Merr.) cultivars differ in their resistance to sudden death syndrome (SDS), caused by Fusarium virguliforme. Breeding for improving SDS response has been challenging, due to interactions among the 18-42 known resistance loci. Four quantitative trait loci (QTL) for resistance to SDS (cqRfs–cqRfs3) were clustered within 20 cM of the rhg1 locus underlying resistance to soybean cyst nematode (SCN) on Chromosome (Chr.) 18. Another locus on Chr. 20 (cqRfs5) was reported to interact with this cluster. The aims here were to compare the inheritance of resistance to SDS in a near isogenic line (NIL) population that was fixed for resistance to SCN but segregated at two of the four loci (cqRfs1 and cqRfs) for SDS resistance; to examine the interaction with the locus on Chr. 20; and to identify candidate genes underlying QTL. Used were; a NIL population derived from residual heterozygosity in an F5:7 recombinant inbred line EF60 (lines 1-38); SDS response data from two locations and years; four segregating microsatellite and 1,500 SNP markers. Polymorphic regions were found from 2,788 Kbp to 8,938 Kbp on Chr. 18 and 33,100 Kbp to 34,943 Kbp on Chr. 20 that were significantly (0.005 < P > 0.0001) associated with resistance to SDS. The QTL fine maps suggested that the two loci on Chr. 18 were three loci (cqRfs1, cqRfs, and cqRfs19). Candidate genes were inferred.  An epistatic interaction was inferred between Chr. 18 and Chr. 20 loci. Therefore, SDS resistance QTL were both complex and interacting.

2020 ◽  
Vol 3 (2) ◽  
pp. 28 ◽  
Author(s):  
Frank M. You ◽  
Sylvie Cloutier

Quantitative trait loci (QTL) are genomic regions associated with phenotype variation of quantitative traits. To date, a total of 313 QTL for 31 quantitative traits have been reported in 14 studies on flax. Of these, 200 QTL from 12 studies were identified based on genetic maps, the scaffold sequences, or the pre-released chromosome-scale pseudomolecules. Molecular markers for QTL identification differed across studies but the most used ones were simple sequence repeats (SSRs) or single nucleotide polymorphisms (SNPs). To uniquely map the SSR and SNP markers from different references onto the recently released chromosome-scale pseudomolecules, methods with several scripts and database files were developed to locate PCR- and SNP-based markers onto the same reference, co-locate QTL, and scan genome-wide candidate genes. Using these methods, 195 out of 200 QTL were successfully sorted onto the 15 flax chromosomes and grouped into 133 co-located QTL clusters; the candidate genes that co-located with these QTL clusters were also predicted. The methods and tools presented in this article facilitate marker re-mapping to a new reference, genome-wide QTL analysis, candidate gene scanning, and breeding applications in flax and other crops.


2015 ◽  
Vol 129 (3) ◽  
pp. 495-506 ◽  
Author(s):  
Sivakumar Swaminathan ◽  
Nilwala S. Abeysekara ◽  
Min Liu ◽  
Silvia R. Cianzio ◽  
Madan K. Bhattacharyya

2006 ◽  
Vol 41 (9) ◽  
pp. 1385-1391 ◽  
Author(s):  
Naoki Yamanaka ◽  
Francisco Horacio Fuentes ◽  
Javier Ramon Gilli ◽  
Satoshi Watanabe ◽  
Kyuya Harada ◽  
...  

The objective of this work was to identify genomic regions that underlie resistance to Fusarium tucumaniae sp. nov., the causing agent of sudden death syndrome (SDS) in soybean in South America, using a population with a genetic background different from that previously reported for Fusarium virguliforme sp. nov. (F. solani f. sp. glycines), also responsible for SDS in soybean. Although major genes and quantitative trait loci (QTL) for SDS resistance have been identified, little is known about the same disease caused by Fusarium tucumaniae sp. nov., in South America. To identify genetic factors related to resistance to F. tucumaniae and DNA markers associated with them, a QTL analysis was performed using recombinant inbred lines. The map locations of the four loci, here identified, differed from those SDS resistance QTL previously described. It was screened a residual heterozygous line (RHL), which was heterozygous around the most effective QTL, RSDS1, and homozygous for the other genomic regions. The genetic effect of RSDS1 was confirmed using near-isogenic lines (NIL) derived from the RHL. The line which was homozygous for the Misuzudaizu genotype showed resistance levels comparable with that of the line homozygous for the Moshidou Gong 503 genotype.


Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 683-696 ◽  
Author(s):  
Justin O Borevitz ◽  
Julin N Maloof ◽  
Jason Lutes ◽  
Tsegaye Dabi ◽  
Joanna L Redfern ◽  
...  

AbstractWe have mapped quantitative trait loci (QTL) responsible for natural variation in light and hormone response between the Cape Verde Islands (Cvi) and Landsberg erecta (Ler) accessions of Arabidopsis thaliana using recombinant inbred lines (RILs). Hypocotyl length was measured in four light environments: white, blue, red, and far-red light and in the dark. In addition, white light plus gibberellin (GA) and dark plus the brassinosteroid biosynthesis inhibitor brassinazole (BRZ) were used to detect hormone effects. Twelve QTL were identified that map to loci not previously known to affect light response, as well as loci where candidate genes have been identified from known mutations. Some QTL act in all environments while others show genotype-by-environment interaction. A global threshold was established to identify a significant epistatic interaction between two loci that have few main effects of their own. LIGHT1, a major QTL, has been confirmed in a near isogenic line (NIL) and maps to a new locus with effects in all light environments. The erecta mutation can explain the effect of the HYP2 QTL in the blue, BRZ, and dark environments, but not in far-red. LIGHT2, also confirmed in an NIL, has effects in white and red light and shows interaction with GA. The phenotype and map position of LIGHT2 suggest the photoreceptor PHYB as a candidate gene. Natural variation in light and hormone response thus defines both new genes and known genes that control light response in wild accessions.


2005 ◽  
Vol 48 (1) ◽  
pp. 106-112 ◽  
Author(s):  
Hyeun-Kyeung Kim ◽  
Sung-Taeg Kang ◽  
Jun-Hyeun Cho ◽  
Myoung-Gun Choung ◽  
Duck-Yong Suh

Sign in / Sign up

Export Citation Format

Share Document