scholarly journals qMrdd2, a novel quantitative resistance locus for maize rough dwarf disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Weixiao Zhang ◽  
Suining Deng ◽  
Yan Zhao ◽  
Wei Xu ◽  
Qingcai Liu ◽  
...  
Keyword(s):  
Quantitative Trait ◽  
Quantitative Resistance ◽  
Complex Trait ◽  
Maize Yield ◽  
Severity Index ◽  
Resistance Locus ◽  
Chromosome 2 ◽  
Maize Rough Dwarf Disease ◽  
Trait Locus ◽  
Dwarf Disease

Abstract Background Maize rough dwarf disease (MRDD), a widespread disease caused by four pathogenic viruses, severely reduces maize yield and grain quality. Resistance against MRDD is a complex trait that controlled by many quantitative trait loci (QTL) and easily influenced by environmental conditions. So far, many studies have reported numbers of resistant QTL, however, only one QTL have been cloned, so it is especially important to map and clone more genes that confer resistance to MRDD. Results In the study, a major quantitative trait locus (QTL) qMrdd2, which confers resistance to MRDD, was identified and fine mapped. qMrdd2, located on chromosome 2, was consistently identified in a 15-Mb interval between the simple sequence repeat (SSR) markers D184 and D1600 by using a recombinant inbred line (RIL) population derived from a cross between resistant (“80007”) and susceptible (“80044”) inbred lines. Using a recombinant-derived progeny test strategy, qMrdd2 was delineated to an interval of 577 kb flanked by markers N31 and N42. We further demonstrated that qMrdd2 is an incompletely dominant resistance locus for MRDD that reduced the disease severity index by 20.4%. Conclusions A major resistance QTL (qMrdd2) have been identified and successfully refined into 577 kb region. This locus will be valuable for improving maize variety resistance to MRDD via marker-assisted selection (MAS).

Fine mapping of a quantitative trait locus conferring resistance to maize rough dwarf disease

2016 ◽  
Vol 129 (12) ◽  
pp. 2333-2342 ◽  
Author(s):  
Changlin Liu ◽  
Jinge Hua ◽  
Chang Liu ◽  
Degui Zhang ◽  
Zhuanfang Hao ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Fine Mapping ◽  
Quantitative Trait ◽  
Maize Rough Dwarf Disease ◽  
Trait Locus ◽  
Dwarf Disease

scholarly journals Quantitative trait loci associated with susceptibility to therapy-related acute murine promyelocytic leukemia in hCG-PML/RARA transgenic mice

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1434-1442 ◽  
Author(s):  
Ryan K. Funk ◽  
Taylor J. Maxwell ◽  
Masayo Izumi ◽  
Deepa Edwin ◽  
Friederike Kreisel ◽  
...  
Keyword(s):  
Quantitative Trait ◽  
Complex Trait ◽  
Myelogenous Leukemia ◽  
Mouse Strains ◽  
Spleen Weight ◽  
Nucleotide Polymorphisms ◽  
Treatment Regimens ◽  
Multiple Loci ◽  
Acute Myelogenous ◽  
Trait Locus

Abstract Therapy-related acute myelogenous leukemia (t-AML) is an important late adverse effect of alkylator chemotherapy. Susceptibility to t-AML has a genetic component, yet specific genetic variants that influence susceptibility are poorly understood. We analyzed an F2 intercross (n = 282 mice) between mouse strains resistant or susceptible to t-AML induced by the alkylator ethyl-N-nitrosourea (ENU) to identify genes that regulate t-AML susceptibility. Each mouse carried the hCG-PML/RARA transgene, a well-characterized initiator of myeloid leukemia. In the absence of ENU treatment, transgenic F2 mice developed leukemia with higher incidence (79.4% vs 12.5%) and at earlier time points (108 days vs 234 days) than mice in the resistant background. ENU treatment of F2 mice further increased incidence (90.4%) and shortened median survival (171 vs 254 days). We genotyped F2 mice at 384 informative single nucleotide polymorphisms across the genome and performed quantitative trait locus (QTL) analysis. Thirteen QTLs significantly associated with leukemia-free survival, spleen weight, or white blood cell count were identified on 8 chromosomes. These results suggest that susceptibility to ENU-induced leukemia in mice is a complex trait governed by genes at multiple loci. Improved understanding of genetic risk factors should lead to tailored treatment regimens that reduce risk for patients predisposed to t-AML.

A major quantitative trait locus determining serum leptin levels and fat mass is located on human chromosome 2

1997 ◽  
Vol 15 (3) ◽  
pp. 273-276 ◽  
Author(s):  
Anthony G. Comuzzie ◽  
James E. Hixson ◽  
Laura Almasy ◽  
Braxton D. Mitchell ◽  
Michael C. Mahaney ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Human Chromosome ◽  
Fat Mass ◽  
Quantitative Trait ◽  
Major Quantitative Trait Locus ◽  
Chromosome 2 ◽  
Serum Leptin ◽  
Trait Locus

Quantitative trait locus analysis of multiple agronomic traits in the model legume Lotus japonicus

Genome ◽  
2007 ◽  
Vol 50 (7) ◽  
pp. 627-637 ◽  
Author(s):  
Takahiro Gondo ◽  
Shusei Sato ◽  
Kenji Okumura ◽  
Satoshi Tabata ◽  
Ryo Akashi ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Quantitative Trait ◽  
Agronomic Traits ◽  
Recombinant Inbred Lines ◽  
Lotus Japonicus ◽  
Seed Mass ◽  
Chromosome 2 ◽  
Seed Traits ◽  
Model Legume ◽  
Trait Locus

The first quantitative trait locus (QTL) analysis of multiple agronomic traits in the model legume Lotus japonicus was performed with a population of recombinant inbred lines derived from Miyakojima MG-20 × Gifu B-129. Thirteen agronomic traits were evaluated in 2004 and 2005: traits of vegetative parts (plant height, stem thickness, leaf length, leaf width, plant regrowth, plant shape, and stem color), flowering traits (flowering time and degree), and pod and seed traits (pod length, pod width, seeds per pod, and seed mass). A total of 40 QTLs were detected that explained 5%–69% of total variation. The QTL that explained the most variation was that for stem color, which was detected in the same region of chromosome 2 in both years. Some QTLs were colocated, especially those for pod and seed traits. Seed mass QTLs were located at 5 locations that mapped to the corresponding genomic positions of equivalent QTLs in soybean, pea, chickpea, and mung bean. This study provides fundamental information for breeding of agronomically important legume crops.

A major suppressor of cell death, slm1, modifies the expression of the maize (Zea mays L.) lesion mimic mutation les23

Genome ◽  
2004 ◽  
Vol 47 (5) ◽  
pp. 961-969 ◽  
Author(s):  
Bryan W Penning ◽  
Gurmukh S Johal ◽  
Michael D McMullen
Keyword(s):  
Cell Death ◽  
Quantitative Trait ◽  
Chromosome 2 ◽  
Genetic Modifiers ◽  
Lesion Mimic ◽  
Cell Death Pathway ◽  
Delayed Initiation ◽  
Significant Locus ◽  
Trait Locus ◽  
Lesion Severity

Disease lesion mimics provide an excellent biological system to study the genetic basis of cell death in plants. Many lesion mimics show variation in phenotype expression in different genetic backgrounds. Our goal was to identify quantitative trait loci (QTL) modifying lesion mimic expression thereby identifying genetic modifiers of cell death. A recessive lesion mimic, les23, in a severe-expressing line was crossed to the maize inbred line Mo20W, a lesion-suppressing line, and an F2 population was developed for QTL analysis. In addition to locating les23 to the short arm of chromosome 2, this analysis detected significant loci for modification of lesion expression. One highly significant locus was found on the long arm of chromosome 2. The Mo20W allele at this QTL significantly delayed initiation of the lesion phenotype and decreased the final lesion severity. Other QTL with lesser effect affected severity of lesion expression without affecting lesion initiation date. Our results demonstrate that dramatic change in lesion phenotype can be controlled by a single major QTL. The presumed function of this QTL in normal plants is to regulate some aspect of the cell death pathway underlying the les23 phenotype.Key words: genetic background, quantitative trait locus, phenotype suppression, Mo20W, corn.

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