Physical map of the chromosome 6q22 region containing the oculodentodigital dysplasia locus: analysis of thirteen candidate genes and identification of novel ESTs and DNA polymorphisms

2002 ◽  
Vol 98 (1) ◽  
pp. 29-37 ◽  
Author(s):  
S.A. Boyadjiev ◽  
A.B. Chowdry ◽  
R.E. Shapiro ◽  
W.A. Paznekas ◽  
A.E. Wandstrat ◽  
...  
2016 ◽  
Vol 6 (12) ◽  
pp. 3803-3815 ◽  
Author(s):  
Jiafa Chen ◽  
Rosemary Shrestha ◽  
Junqiang Ding ◽  
Hongjian Zheng ◽  
Chunhua Mu ◽  
...  

Abstract Fusarium ear rot (FER) incited by Fusarium verticillioides is a major disease of maize that reduces grain quality globally. Host resistance is the most suitable strategy for managing the disease. We report the results of genome-wide association study (GWAS) to detect alleles associated with increased resistance to FER in a set of 818 tropical maize inbred lines evaluated in three environments. Association tests performed using 43,424 single-nucleotide polymorphic (SNPs) markers identified 45 SNPs and 15 haplotypes that were significantly associated with FER resistance. Each associated SNP locus had relatively small additive effects on disease resistance and accounted for 1–4% of trait variation. These SNPs and haplotypes were located within or adjacent to 38 candidate genes, 21 of which were candidate genes associated with plant tolerance to stresses, including disease resistance. Linkage mapping in four biparental populations to validate GWAS results identified 15 quantitative trait loci (QTL) associated with F. verticillioides resistance. Integration of GWAS and QTL to the maize physical map showed eight colocated loci on chromosomes 2, 3, 4, 5, 9, and 10. QTL on chromosomes 2 and 9 are new. These results reveal that FER resistance is a complex trait that is conditioned by multiple genes with minor effects. The value of selection on identified markers for improving FER resistance is limited; rather, selection to combine small effect resistance alleles combined with genomic selection for polygenic background for both the target and general adaptation traits might be fruitful for increasing FER resistance in maize.


Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1797-1816 ◽  
Author(s):  
Hafid Laayouni ◽  
Mauro Santos ◽  
Antonio Fontdevila

Abstract We present a physical map based on RAPD polymorphic fragments and sequence-tagged sites (STSs) for the repleta group species Drosophila buzzatii. One hundred forty-four RAPD markers have been used as probes for in situ hybridization to the polytene chromosomes, and positive results allowing the precise localization of 108 RAPDs were obtained. Of these, 73 behave as effectively unique markers for physical map construction, and in 9 additional cases the probes gave two hybridization signals, each on a different chromosome. Most markers (68%) are located on chromosomes 2 and 4, which partially agree with previous estimates on the distribution of genetic variation over chromosomes. One RAPD maps close to the proximal breakpoint of inversion 2z3 but is not included within the inverted fragment. However, it was possible to conclude from this RAPD that the distal breakpoint of 2z3 had previously been wrongly assigned. A total of 39 cytologically mapped RAPDs were converted to STSs and yielded an aggregate sequence of 28,431 bp. Thirty-six RAPDs (25%) did not produce any detectable hybridization signal, and we obtained the DNA sequence from three of them. Further prospects toward obtaining a more developed genetic map than the one currently available for D. buzzatii are discussed.


2008 ◽  
Vol 8 (1) ◽  
pp. 66 ◽  
Author(s):  
Marco Moroldo ◽  
Sophie Paillard ◽  
Raffaella Marconi ◽  
Legeai Fabrice ◽  
Aurelie Canaguier ◽  
...  

2008 ◽  
Vol 34 (1) ◽  
pp. 42-53 ◽  
Author(s):  
Christian Schmidt ◽  
Nina P. Gonzaludo ◽  
Sarah Strunk ◽  
Stefan Dahm ◽  
Johannes Schuchhardt ◽  
...  

Crossbreeding studies in rodents have identified numerous quantitative trait loci (QTL) that are linked to diabetes-related component traits. To identify genetic consensus regions implicated in insulin action and glucose homeostasis, we have performed a meta-analysis of genomewide linkage scans for diabetes-related traits. From a total of 43 published genomewide scans we assembled a nonredundant collection of 153 QTL for glucose levels, insulin levels, and glucose tolerance. Collectively, these studies include data from 48 different parental strains and >11,000 individual animals. The results of the studies were analyzed by the truncated product method (TPM). The analysis revealed significant evidence for linkage of glucose levels, insulin levels, and glucose tolerance to 27 different segments of the mouse genome. The most prominent consensus regions [localized to chromosomes 2, 4, 7, 9, 11, 13, and 19; logarithm of odds (LOD) scores 10.5–17.4] cover ∼11% of the mouse genome and collectively contain the peak markers for 47 QTL. Approximately half of these genomic segments also show significant linkage to body weight and adiposity, indicating the presence of multiple obesity-dependent and -independent consensus regions for diabetes-related traits. At least 84 human genetic markers from genomewide scans and >80 candidate genes from human and rodent studies map into the mouse consensus regions for diabetes-related traits, indicating a substantial overlap between the species. Our results provide guidance for the identification of novel candidate genes and demonstrate the presence of numerous distinct consensus QTL regions with highly significant LOD scores that control glucose homeostasis. An interactive physical map of the QTL is available online at http://www.diabesitygenes.org .


Genome ◽  
1989 ◽  
Vol 32 (3) ◽  
pp. 365-372 ◽  
Author(s):  
T. Starr ◽  
A. M. Howell ◽  
J. McDowall ◽  
K. Peters ◽  
A. M. Rose

We have isolated probes for DNA polymorphisms across the linkage group I gene cluster in Caenorhabditis elegans, using Tc1-linkage selection. The probes detect strain polymorphism between the wild-type strains of var. Bristol and var. Bergerac. As a result of mapping the sites hP4, hP5, hP6, hP7, hP9, and sP1, more than 1000 kilobases (kb) of cloned cosmid DNA has been positioned on the genetic map. We found there is more DNA per map unit in the center of the gene cluster than expected on the basis of the genomic average. Furthermore, the amount is not constant across the entire region but reaches a peak in the hP9 unc-13 interval. To find the coding regions, we examined DNA cross-homology between two species, Caenorhabditis elegans and Caenorhabditis briggsae. Approximately one-third of the DNA in the hP5 hP9 interval was examined for coding regions and 21 sequences were identified within 318 kb of DNA.Key words: Caenorhabditis elegans, physical map, DNA polymorphisms, genetic mapping, Caenorhabditis briggsae.


2013 ◽  
Vol 28 (S2) ◽  
pp. 21-21
Author(s):  
N. Ramoz

Anorexia Nervosa (AN) is a young-onset psychiatric illness, for which the etiology remains unknown and presents a high heritability. Thus, the genetic component is estimated to be 70%. To identify the vulnerability genes to AN, different approaches of molecular genetic are performed, including linkage analysis, the candidate gene association study and, the Genome-Wide Association Study (GWAS). Some polymorphisms of candidate genes, such as the BDNF gene that encodes for the brain-derived neurotrophic factor, were found associated with AN in several studies. In addition to the DNA polymorphisms, there are several other changes around the DNA information, like methylation or the histone modifications, named epigenetic, that modulate the transcription of genes. Thus, first descendents after the Dutch famine in the Second World War have showed a higher risk of impaired glucose tolerance in adulthood. And women exposed to famine in utero presented DNA methylation differences but without link of cause or consequence between famine event and epigenetic changes. To date, only few events of methylation in specific candidate genes have been investigated in AN. Thus, an hypermethylation of the DRD2 gene's promoter was found associated with a downregulation of this gene expression in AN compared to healthy control women (HCW), using leucocytes. While a hypermethylation of the DAT1 promoter was observed correlated with an upregulation of this gene expression. Another study has showed no difference of the methylation level of the Proopiomelanocortin (POMC) promoter between the goups of HCW, underweight AN (acAN) and weight-recovered AN (recAN). But, the expression of POMC was significantly higher in acAN compared to recAN and HCW, and correlated with the leptin levels. These studies suggest that both the etiology and the pathologic consequences of AN could be derived by epigenetic factors, such as the methylation.


2018 ◽  
Vol 11 (3) ◽  
pp. 537-550 ◽  
Author(s):  
Jun-Jun Liu ◽  
Simon Francis Shamoun ◽  
Isabel Leal ◽  
Robert Kowbel ◽  
Grace Sumampong ◽  
...  

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