scholarly journals Identification and Mapping of Quantitative Trait Loci Conditioning Resistance to Southern Leaf Blight of Maize Caused by Cochliobolus heterostrophus Race O

2004 ◽  
Vol 94 (8) ◽  
pp. 862-867 ◽  
Author(s):  
M. L. Carson ◽  
C. W. Stuber ◽  
M. L. Senior

A random set of recombinant inbred (RI) lines (F2:7) derived from the cross of the inbred lines Mo17 (resistant) and B73 (susceptible) were evaluated for resistance to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O. The RI lines were genotyped at a total of 234 simple sequence repeat, restriction fragment length polymorphism, or isozyme loci. Field plots of the RI lines were inoculated artificially with an aggressive isolate of C. heterostrophus race O in each of two growing seasons in North Carolina. Lines were rated for percent SLB severity two (1996) or three (1995) times during the grain-filling period. Data also were converted to area under the disease progress curve (AUDPC) and analyzed using the composite interval mapping option of the PLABQTL program. When means of disease ratings over years were fitted to models, a total of 11 quantitative trait loci (QTLs) were found to condition resistance to SLB, depending upon which disease ratings were used in the analyses. When the AUDPC data were combined and analyzed over environments, seven QTLs, on chromosomes 1, 2, 3, 4, 7, and 10 were found to come from the resistant parent Mo17. An additional QTL for resistance on chromosome 1 came from the susceptible parent B73. The eight identified QTLs accounted for 46% of the phenotypic variation for resistance. QTL × environment interactions often were highly significant but, with one exception, were the result of differences in the magnitude of QTL effects between years and not due to changes in direction of effects. QTLs on the long arm of chromosome 1 and chromosomes 2 and 3 had the largest effects, were the most consistently detected, and accounted for most of the phenotypic variance. No significant additive × additive epistatic effects were detected. These data support earlier reports of the polygenic inheritance of resistance to SLB of maize.

2019 ◽  
Vol 167 (10) ◽  
pp. 591-600 ◽  
Author(s):  
Maninder Kaur ◽  
Yogesh Vikal ◽  
Harleen Kaur ◽  
Lalit Pal ◽  
Kirandeep Kaur ◽  
...  

Genes ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 62
Author(s):  
Niranjan Baisakh ◽  
Jonalyn Yabes ◽  
Andres Gutierrez ◽  
Venkata Mangu ◽  
Peiyong Ma ◽  
...  

Improving drought resistance in crops is imperative under the prevailing erratic rainfall patterns. Drought affects the growth and yield of most modern rice varieties. Recent breeding efforts aim to incorporate drought resistance traits in rice varieties that can be suitable under alternative irrigation schemes, such as in a (semi)aerobic system, as row (furrow-irrigated) rice. The identification of quantitative trait loci (QTLs) controlling grain yield, the most important trait with high selection efficiency, can lead to the identification of markers to facilitate marker-assisted breeding of drought-resistant rice. Here, we report grain yield QTLs under greenhouse drought using an F2:3 population derived from Cocodrie (drought sensitive) × Nagina 22 (N22) (drought tolerant). Eight QTLs were identified for yield traits under drought. Grain yield QTL under drought on chromosome 1 (phenotypic variance explained (PVE) = 11.15%) co-localized with the only QTL for panicle number (PVE = 37.7%). The drought-tolerant parent N22 contributed the favorable alleles for all QTLs except qGN3.2 and qGN5.1 for grain number per panicle. Stress-responsive transcription factors, such as ethylene response factor, WD40 domain protein, zinc finger protein, and genes involved in lipid/sugar metabolism were linked to the QTLs, suggesting their possible role in drought tolerance mechanism of N22 in the background of Cocodrie, contributing to higher yield under drought.


2008 ◽  
Vol 98 (3) ◽  
pp. 315-320 ◽  
Author(s):  
P. J. Balint-Kurti ◽  
J. C. Zwonitzer ◽  
M. E. Pè ◽  
G. Pea ◽  
M. Lee ◽  
...  

The genetic architecture underlying resistance in maize to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O is not well understood. The objective of this study was to identify loci contributing to SLB resistance in two recombinant inbred line populations and to compare these to SLB resistance loci in other populations. The two populations used were derived from crosses between maize inbred lines H99 and B73 (HB population–142 lines) and between B73 and B52 (BB population–186 lines). They were evaluated for SLB resistance and for days from planting to anthesis (DTA) in 2005 and 2006. Two replications arranged as randomized complete blocks were assessed in each year for each population. Entry mean heritabilities for disease resistance were high for both populations (0.876 and 0.761, respectively). Quantitative trait loci (QTL) for SLB resistance were identified in bins 3.04 (two QTL), 6.01, and 8.05 in the HB population and in bin 2.07 in the BB population. No overlap of DTA and SLB resistance QTL was observed, nor was there any phenotypic correlation between the traits. A comparison of the results of all published SLB resistance QTL studies suggested that bins 3.04 and 6.01 are ‘hotspots’ for SLB resistance QTL.


2006 ◽  
Vol 96 (3) ◽  
pp. 221-225 ◽  
Author(s):  
P. J. Balint-Kurti ◽  
M. L. Carson

A set of 192 maize recombinant inbred lines (RILs), derived from a cross between the inbred lines Mo17 and B73, were evaluated as 3-week-old seedlings in the greenhouse for resistance to southern leaf blight, caused by Cochliobolus heterostrophus race O. Six significant (LOD >3.1) quantitative trait loci (QTL) were identified for disease resistance, located on chromosomes 1, 2, 3, 6, 7, and 8. Results were compared with a previous study that had used the same RIL population and pathogen isolate, but had examined resistance in mature rather than juvenile plants. There was a very weak but significant correlation between the overall resistance phenotypes of the RILs scored as mature and juvenile plants. Two QTL were found in similar positions on chromosomes 1 and 3 at both growth stages. Other QTL were specific to one growth stage or the other. Twenty-three of these RILs, together with the parental lines, were inoculated in the greenhouse with four C. heterostrophus isolates. Results indicated that the quantitative resistance observed was largely isolate non-specific.


2012 ◽  
Vol 52 (11) ◽  
pp. 1012 ◽  
Author(s):  
S. S. Sohrabi ◽  
A. K. Esmailizadeh ◽  
A. Baghizadeh ◽  
H. Moradian ◽  
M. R. Mohammadabadi ◽  
...  

A three-generation resource population was developed using two distinct Japanese quail strains, wild and white, to map quantitative trait loci underlying hatching weight and growth traits. Eight pairs of white and wild birds were crossed reciprocally and 34 F1 birds were produced. The F1 birds were intercrossed to generate 422 F2 offspring. All of the animals from three generations (472 birds) were genotyped for eight microsatellite markers on chromosome 1. Liveweight data from hatch to 5 weeks of age were collected on the F2 birds. Quantitative trait loci (QTL) analysis was conducted applying the line-cross model and the least-squares interval mapping approach. The results indicated QTL affecting hatching weight and several growth related traits on chromosome 1. The F2 phenotypic variance explained by the detected additive QTL effects ranged from 1.0 to 3.7 for different traits. Modelling both additive and dominance QTL effects revealed additional QTL with significant dominance mode of action affecting pre-slaughter weight. However, there was no evidence for imprinting (parent-of-origin) effects. The variance due to the reciprocal cross effect ranged between 3.0 and 19.1% for weight at 1 week of age and hatching weight, respectively.


2006 ◽  
Vol 96 (10) ◽  
pp. 1067-1071 ◽  
Author(s):  
P. J. Balint-Kurti ◽  
M. D. Krakowsky ◽  
M. P. Jines ◽  
L. A. Robertson ◽  
T. L. Molnár ◽  
...  

A recombinant inbred line population derived from a cross between the maize lines NC300 (resistant) and B104 (susceptible) was evaluated for resistance to southern leaf blight (SLB) disease caused by Cochliobolus heterostrophus race O and for days to anthesis in four environments (Clayton, NC, and Tifton, GA, in both 2004 and 2005). Entry mean and average genetic correlations between disease ratings in different environments were high (0.78 to 0.89 and 0.9, respectively) and the overall entry mean heritability for SLB resistance was 0.89. When weighted mean disease ratings were fitted to a model using multiple interval mapping, seven potential quantitative trait loci (QTL) were identified, the two strongest being on chromosomes 3 (bin 3.04) and 9 (bin 9.03–9.04). These QTL explained a combined 80% of the phenotypic variation for SLB resistance. Some time-point-specific SLB resistance QTL were also identified. There was no significant correlation between disease resistance and days to anthesis. Six putative QTL for time to anthesis were identified, none of which coincided with any SLB resistance QTL.


Genetics ◽  
1999 ◽  
Vol 152 (2) ◽  
pp. 699-711 ◽  
Author(s):  
D E Moody ◽  
D Pomp ◽  
M K Nielsen ◽  
L D Van Vleck

Abstract Energy balance is a complex trait with relevance to the study of human obesity and maintenance energy requirements of livestock. The objective of this study was to identify, using unique mouse models, quantitative trait loci (QTL) influencing traits that contribute to variation in energy balance. Two F2 resource populations were created from lines of mice differing in heat loss measured by direct calorimetry as an indicator of energy expenditure. The HB F2 resource population originated from a cross between a noninbred line selected for high heat loss and an inbred line with low heat loss. Evidence for significant QTL influencing heat loss was found on chromosomes 1, 2, 3, and 7. Significant QTL influencing body weight and percentage gonadal fat, brown fat, liver, and heart were also identified. The LH F2 resource population originated from noninbred lines of mice that had undergone divergent selection for heat loss. Chromosomes 1 and 3 were evaluated. The QTL for heat loss identified on chromosome 1 in the HB population was confirmed in the LH population, although the effect was smaller. The presence of a QTL influencing 6-wk weight was also confirmed. Suggestive evidence for additional QTL influencing heat loss, percentage subcutaneous fat, and percentage heart was found for chromosome 1.


Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1307-1315
Author(s):  
Daibin Zhong ◽  
Aditi Pai ◽  
Guiyun Yan

Abstract Parasites have profound effects on host ecology and evolution, and the effects of parasites on host ecology are often influenced by the magnitude of host susceptibility to parasites. Many parasites have complex life cycles that require intermediate hosts for their transmission, but little is known about the genetic basis of the intermediate host's susceptibility to these parasites. This study examined the genetic basis of susceptibility to a tapeworm (Hymenolepis diminuta) in the red flour beetle (Tribolium castaneum) that serves as an intermediate host in its transmission. Quantitative trait loci (QTL) mapping experiments were conducted with two independent segregating populations using amplified fragment length polymorphism (AFLP) markers and randomly amplified polymorphic DNA (RAPD) markers. A total of five QTL that significantly affected beetle susceptibility were identified in the two reciprocal crosses. Two common QTL on linkage groups 3 and 6 were identified in both crosses with similar effects on the phenotype, and three QTL were unique to each cross. In one cross, the three main QTL accounted for 29% of the total phenotypic variance and digenic epistasis explained 39% of the variance. In the second cross, the four main QTL explained 62% of the variance and digenic epistasis accounted for only 5% of the variance. The actions of these QTL were either overdominance or underdominance. Our results suggest that the polygenic nature of beetle susceptibility to the parasites and epistasis are important genetic mechanisms for the maintenance of variation within or among beetle strains in susceptibility to tapeworm infection.


Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 673-684
Author(s):  
J Gadau ◽  
R E Page ◽  
J H Werren

Abstract There is a 2.5-fold difference in male wing size between two haplodiploid insect species, Nasonia vitripennis and N. giraulti. The haploidy of males facilitated a full genomic screen for quantitative trait loci (QTL) affecting wing size and the detection of epistatic interactions. A QTL analysis of the interspecific wing-size difference revealed QTL with major effects and epistatic interactions among loci affecting the trait. We analyzed 178 hybrid males and initially found two major QTL for wing length, one for wing width, three for a normalized wing-size variable, and five for wing seta density. One QTL for wing width explains 38.1% of the phenotypic variance, and the same QTL explains 22% of the phenotypic variance in normalized wing size. This corresponds to a region previously introgressed from N. giraulti into N. vitripennis that accounts for 44% of the normalized wing-size difference between the species. Significant epistatic interactions were also found that affect wing size and density of setae on the wing. Screening for pairwise epistatic interactions between loci on different linkage groups revealed four additional loci for wing length and four loci for normalized wing size that were not detected in the original QTL analysis. We propose that the evolution of smaller wings in N. vitripennis males is primarily the result of major mutations at few genomic regions and involves epistatic interactions among some loci.


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