scholarly journals Genomic Locus Modulating IOP in the BXD RI Mouse Strains

2017 ◽  
Author(s):  
Rebecca King ◽  
Ying Li ◽  
Jiaxing Wang ◽  
Felix L. Struebing ◽  
Eldon E. Geisert
Keyword(s):  
Candidate Genes ◽  
Quantitative Trait ◽  
Significant Quantitative Trait Locus ◽  
Interval Mapping ◽  
Mouse Strains ◽  
Genomic Locus ◽  
Quantitative Trait Analysis ◽  
Significant Locus ◽  
Trait Locus ◽  
Different Strains

AbstractPurposeIntraocular pressure (IOP) is the primary risk factor for developing glaucoma. The present study examines genomic contribution to the normal regulation of IOP in the mouse.MethodsThe BXD recombinant inbred (RI) strain set was used to identify genomic loci modulating IOP. We measured the IOP from 532 eyes from 34 different strains. The IOP data will be subjected to conventional quantitative trait analysis using simple and composite interval mapping along with epistatic interactions to define genomic loci modulating normal IOP.ResultsThe analysis defined one significant quantitative trait locus (QTL) on Chr.8 (100 to 106 Mb). The significant locus was further examined to define candidate genes that modulate normal IOP. There are only two good candidate genes within the 6 Mb over the peak, Cdh8 (Cadherin 8) and Cdh11 (Cadherin 11). Expression analysis on gene expression and immunohistochemistry indicate that Cdh11 is the best candidate for modulating the normal levels of IOP.ConclusionsWe have examined the genomic regulation of IOP in the BXD RI strain set and found one significant QTL on Chr. 8. Within this QTL that are two potential candidates for modulating IOP with the most likely gene being Cdh11.

scholarly journals Genomic Locus Modulating IOP in the BXD RI Mouse Strains

2017 ◽  
Author(s):  
Rebecca King ◽  
Ying Li ◽  
Jiaxing Wang ◽  
Felix L. Struebing ◽  
Eldon E. Geisert
Keyword(s):  
Candidate Genes ◽  
Quantitative Trait ◽  
Significant Quantitative Trait Locus ◽  
Interval Mapping ◽  
Mouse Strains ◽  
Genomic Locus ◽  
Quantitative Trait Analysis ◽  
Significant Locus ◽  
Trait Locus ◽  
Different Strains

AbstractPurposeIntraocular pressure (IOP) is the primary risk factor for developing glaucoma. The present study examines genomic contribution to the normal regulation of IOP in the mouse.MethodsThe BXD recombinant inbred (RI) strain set was used to identify genomic loci modulating IOP. We measured the IOP from 532 eyes from 33 different strains. The IOP data will be subjected to conventional quantitative trait analysis using simple and composite interval mapping along with epistatic interactions to define genomic loci modulating normal IOP.ResultsThe analysis defined one significant quantitative trait locus (QTL) on Chr.8 (100 to 106 Mb). The significant locus was further examined to define candidate genes that modulate normal IOP. There are only two good candidate genes within the 6 Mb over the peak, Cdh8 (Cadherin 8) and Cdh11 (Cadherin 11). Expression analysis on gene expression and immunohistochemistry indicate that Cdh11 is the best candidate for modulating the normal levels of IOP.ConclusionsWe have examined the genomic regulation of IOP in the BXD RI strain set and found one significant QTL on Chr. 8. Within this QTL that are two potential candidates for modulating IOP with the most likely gene being Cdh11.

scholarly journals Integration and Modularity of Quantitative Trait Locus Effects on Geometric Shape in the Mouse Mandible

Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1909-1921
Author(s):  
Christian Peter Klingenberg ◽  
Larry J Leamy ◽  
James M Cheverud
Keyword(s):  
Quantitative Trait ◽  
Parametric Bootstrap ◽  
Interval Mapping ◽  
Procrustes Analysis ◽  
Bootstrap Test ◽  
Mandible Shape ◽  
Trait Locus ◽  
F2 Generation ◽  
Analysis Interval ◽  
Qtl Effects

Abstract The mouse mandible has long served as a model system for complex morphological structures. Here we use new methodology based on geometric morphometrics to test the hypothesis that the mandible consists of two main modules, the alveolar region and the ascending ramus, and that this modularity is reflected in the effects of quantitative trait loci (QTL). The shape of each mandible was analyzed by the positions of 16 morphological landmarks and these data were analyzed using Procrustes analysis. Interval mapping in the F2 generation from intercrosses of the LG/J and SM/J strains revealed 33 QTL affecting mandible shape. The QTL effects corresponded to a variety of shape changes, but ordination or a parametric bootstrap test of clustering did not reveal any distinct groups of QTL that would affect primarily one module or the other. The correlations of landmark positions between the two modules tended to be lower than the correlations between arbitrary subsets of landmarks, indicating that the modules were relatively independent of each other and confirming the hypothesized location of the boundary between them. While these results are in agreement with the hypothesis of modularity, they also underscore that modularity is a question of the relative degrees to which QTL contribute to different traits, rather than a question of discrete sets of QTL contributing to discrete sets of traits.

scholarly journals Transcriptomic profiling of wheat near-isogenic lines reveals candidate genes on chromosome 3A for pre-harvest sprouting resistance

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xingyi Wang ◽  
Hui Liu ◽  
Kadambot H. M. Siddique ◽  
Guijun Yan
Keyword(s):  
Candidate Genes ◽  
Quantitative Trait ◽  
Genomic Region ◽  
Nucleotide Polymorphisms ◽  
Near Isogenic Lines ◽  
Gene Effects ◽  
Isogenic Lines ◽  
Trait Locus ◽  
Grain Yield And Quality ◽  
Sprouting Resistance

Abstract Background Pre-harvest sprouting (PHS) in wheat can cause severe damage to both grain yield and quality. Resistance to PHS is a quantitative trait controlled by many genes located across all 21 wheat chromosomes. The study targeted a large-effect quantitative trait locus (QTL) QPhs.ccsu-3A.1 for PHS resistance using several sets previously developed near-isogenic lines (NILs). Two pairs of NILs with highly significant phenotypic differences between the isolines were examined by RNA sequencing for their transcriptomic profiles on developing seeds at 15, 25 and 35 days after pollination (DAP) to identify candidate genes underlying the QTL and elucidate gene effects on PHS resistance. At each DAP, differentially expressed genes (DEGs) between the isolines were investigated. Results Gene ontology and KEGG pathway enrichment analyses of key DEGs suggested that six candidate genes underlie QPhs.ccsu-3A.1 responsible for PHS resistance in wheat. Candidate gene expression was further validated by quantitative RT-PCR. Within the targeted QTL interval, 16 genetic variants including five single nucleotide polymorphisms (SNPs) and 11 indels showed consistent polymorphism between resistant and susceptible isolines. Conclusions The targeted QTL is confirmed to harbor core genes related to hormone signaling pathways that can be exploited as a key genomic region for marker-assisted selection. The candidate genes and SNP/indel markers detected in this study are valuable resources for understanding the mechanism of PHS resistance and for marker-assisted breeding of the trait in wheat.

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.

scholarly journals Analysis of candidate genes for morphine preference quantitative trait locus Mop2

Neuroscience ◽  
2014 ◽  
Vol 277 ◽  
pp. 403-416 ◽  
Author(s):  
G.A. Doyle ◽  
C.L. Schwebel ◽  
S.E. Ruiz ◽  
A.D. Chou ◽  
A.T. Lai ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Candidate Genes ◽  
Quantitative Trait ◽  
Trait Locus

scholarly journals Genetic Mapping with Background Control for Quantitative Trait Locus (QTL) in 8-Parental Pure-Line Populations

2019 ◽  
Vol 110 (7) ◽  
pp. 880-891 ◽  
Author(s):  
Jinhui Shi ◽  
Jiankang Wang ◽  
Luyan Zhang
Keyword(s):  
Quantitative Trait Locus ◽  
Genetic Variation ◽  
Linear Model ◽  
Quantitative Trait ◽  
Genetic Model ◽  
Pure Line ◽  
Interval Mapping ◽  
Unbiased Estimation ◽  
Trait Locus ◽  
Marker Variables

Abstract Multiparental advanced generation intercross (MAGIC) populations provide abundant genetic variation for use in plant genetics and breeding. In this study, we developed a method for quantitative trait locus (QTL) detection in pure-line populations derived from 8-way crosses, based on the principles of inclusive composite interval mapping (ICIM). We considered 8 parents carrying different alleles with different effects. To estimate the 8 genotypic effects, 1-locus genetic model was first built. Then, an orthogonal linear model of phenotypes against marker variables was established to explain genetic effects of the locus. The linear model was estimated by stepwise regression and finally used for phenotype adjustment and background genetic variation control in QTL mapping. Simulation studies using 3 genetic models demonstrated that the proposed method had higher detection power, lower false discovery rate (FDR), and unbiased estimation of QTL locations compared with other methods. Marginal bias was observed in the estimation of QTL effects. An 8-parental recombinant inbred line (RIL) population previously reported in cowpea and analyzed by interval mapping (IM) was reanalyzed by ICIM and genome-wide association mapping implemented in software FarmCPU. The results indicated that ICIM identified more QTLs explaining more phenotypic variation than did IM; ICIM provided more information on the detected QTL than did FarmCPU; and most QTLs identified by IM and FarmCPU were also detected by ICIM.

scholarly journals New quantitative trait loci for carotid atherosclerosis identified in an intercross derived from apolipoprotein E-deficient mouse strains

2013 ◽  
Vol 45 (8) ◽  
pp. 332-342 ◽  
Author(s):  
Jessica S. Rowlan ◽  
Zhimin Zhang ◽  
Qian Wang ◽  
Yan Fang ◽  
Weibin Shi
Keyword(s):  
Apolipoprotein E ◽  
Quantitative Trait ◽  
Carotid Atherosclerosis ◽  
Plasma Lipid ◽  
Hdl Cholesterol ◽  
Carotid Bifurcation ◽  
Mouse Strains ◽  
Entire Genome ◽  
Significant Qtls ◽  
Trait Locus

Carotid atherosclerosis is the primary cause of ischemic stroke. To identify genetic factors contributing to carotid atherosclerosis, we performed quantitative trait locus (QTL) analysis using female mice derived from an intercross between C57BL/6J (B6) and BALB/cJ (BALB) apolipoprotein E ( Apoe−/−) mice. We started 266 F2 mice on a Western diet at 6 wk of age and fed them the diet for 12 wk. Atherosclerotic lesions in the left carotid bifurcation and plasma lipid levels were measured. We genotyped 130 microsatellite markers across the entire genome. Three significant QTLs, Cath1 on chromosome (Chr) 12, Cath2 on Chr5, and Cath3 on Chr13, and four suggestive QTLs on Chr6, Chr9, Chr17, and Chr18 were identified for carotid lesions. The Chr6 locus replicated a suggestive QTL and was named Cath4. Six QTLs for HDL, three QTLs for non-HDL cholesterol, and three QTLs for triglyceride were found. Of these, a significant QTL for non-HDL on Chr1 at 60.3 cM, named Nhdl13, and a suggestive QTL for HDL on ChrX were new. A significant locus for HDL ( Hdlq5) was overlapping with a suggestive locus for carotid lesions on Chr9. A significant correlation between carotid lesion sizes and HDL cholesterol levels was observed in the F2 population ( R = −0.153, P = 0.0133). Thus, we have identified several new QTLs for carotid atherosclerosis and the locus on Chr9 may exert effect through interactions with HDL.

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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