Gotowe bibliografie tematyczne / Genetic loci

Gotowa bibliografia na temat „Genetic loci”

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Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 września 2023

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Artykuły w czasopismach na temat "Genetic loci"

1

Ott, Jurg. "Association of genetic loci". Neurology 63, nr 6 (27.09.2004): 955–58. http://dx.doi.org/10.1212/wnl.63.6.955.

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Bhidayasiri, Roongroj, i Stefan-M. Pulst. "Dystonia (DYT) genetic loci". European Journal of Paediatric Neurology 9, nr 5 (wrzesień 2005): 367–70. http://dx.doi.org/10.1016/j.ejpn.2005.05.002.

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Rajon, Etienne, i Joshua B. Plotkin. "The evolution of genetic architectures underlying quantitative traits". Proceedings of the Royal Society B: Biological Sciences 280, nr 1769 (22.10.2013): 20131552. http://dx.doi.org/10.1098/rspb.2013.1552.

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In the classic view introduced by R. A. Fisher, a quantitative trait is encoded by many loci with small, additive effects. Recent advances in quantitative trait loci mapping have begun to elucidate the genetic architectures underlying vast numbers of phenotypes across diverse taxa, producing observations that sometimes contrast with Fisher's blueprint. Despite these considerable empirical efforts to map the genetic determinants of traits, it remains poorly understood how the genetic architecture of a trait should evolve, or how it depends on the selection pressures on the trait. Here, we develop a simple, population-genetic model for the evolution of genetic architectures. Our model predicts that traits under moderate selection should be encoded by many loci with highly variable effects, whereas traits under either weak or strong selection should be encoded by relatively few loci. We compare these theoretical predictions with qualitative trends in the genetics of human traits, and with systematic data on the genetics of gene expression levels in yeast. Our analysis provides an evolutionary explanation for broad empirical patterns in the genetic basis for traits, and it introduces a single framework that unifies the diversity of observed genetic architectures, ranging from Mendelian to Fisherian.
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4

Medina-Macedo, L., Andre Eduardo Biscaia Lacerda, J. Zanetti Ribeiro, J. V. M. Bittencourt i A. M. Sebbenn. "Investigating the Mendelian inheritance, genetic linkage, and genotypic disequilibrium for ten microsatellite loci of Araucaria angustifolia". Silvae Genetica 63, nr 1-6 (1.12.2014): 234–39. http://dx.doi.org/10.1515/sg-2014-0030.

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AbstractAraucaria angustifolia is a dioecious and wind pollinated conifer that typically occurs in higher attitudes of Southern Brazil. After a significant reduction of its population during the twentieth century, public policies have enabled natural populations to recover. As new studies focus on the genetics of the species it is important to investigate Mendelian inheritance, genetic linkage, and genotypic disequilibrium for the microsatellite loci developed for the species. Here we analyze ten microsatellite loci developed for A. angustifolia by genotyping 295 adult trees and 13 open pollinated progenies from a forest fragment in Santa Catarina, Brazil. The likelihood G-test shows a perfect 1:1 Mendelian segregation for all ten loci, indicating that these molecular markers are genetic markers. Significant genetic linkage between pairwise loci was detected in only 3% of the tests, suggesting that these loci are not located in the same linkage groups within the chromosomes. However, genotypic disequilibrium was detected in 51% of pairwise loci for adult trees, probably due to the strong spatial genetic structure of the population. Our results indicate that the ten loci analyzed can be used in studies on genetic diversity and structure, mating system, and gene flow of the species.
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5

JOOST, OSCAR, JEMMA B WILK, L. ADRIENNE CUPPLES, MICHAEL HARMON, AMANDA M SHEARMAN, CLINTON T BALDWIN, GEORGE T O'CONNOR, RICHARD H MYERS i DANIEL J GOTTLIEB. "Genetic Loci Influencing Lung Function". American Journal of Respiratory and Critical Care Medicine 165, nr 6 (15.03.2002): 795–99. http://dx.doi.org/10.1164/ajrccm.165.6.2102057.

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Schwab, M., R. Corvi i L. Savelyeva. "New Genetic Loci in Neuroblastoma". Klinische Pädiatrie 209, nr 04 (lipiec 1997): 147–49. http://dx.doi.org/10.1055/s-2008-1043966.

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Rustam Singh, Maishnam, i T. Shyamacharan Singh. "Genetic Polymorphisms at three Loci in two Populations of Manipur, India". Anthropologischer Anzeiger 66, nr 2 (11.07.2008): 191–98. http://dx.doi.org/10.1127/aa/66/2008/191.

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Yan, Guiyun, Dave D. Chadee i David W. Severson. "Evidence for Genetic Hitchhiking Effect Associated With Insecticide Resistance in Aedes aegypti". Genetics 148, nr 2 (1.02.1998): 793–800. http://dx.doi.org/10.1093/genetics/148.2.793.

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Abstract Information on genetic variation within and between populations is critical for understanding the evolutionary history of mosquito populations and disease epidemiology. Previous studies with Drosophila suggest that genetic variation of selectively neutral loci in a large fraction of genome may be constrained by fixation of advantageous mutations associated with hitchhiking effect. This study examined restriction fragment length polymorphisms of four natural Aedes aegypti mosquito populations from Trinidad and Tobago, at 16 loci. These populations have been subjected to organophosphate (OP) insecticide treatments for more than two decades, while dichlor-diphenyltrichlor (DDT) was the insecticide of choice prior to this period. We predicted that genes closely linked to the OP target loci would exhibit reduced genetic variation as a result of the hitchhiking effect associated with intensive OP insecticide selection. We also predicted that genetic variability of the genes conferring resistance to DDT and loci near the target site would be similar to other unlinked loci. As predicted, reduced genetic variation was found for loci in the general chromosomal region of a putative OP target site, and these loci generally exhibited larger FST values than other random loci. In contrast, the gene conferring resistance to DDT and its linked loci show polymorphisms and genetic differentiation similar to other random loci. The reduced genetic variability and apparent gene deletion in some regions of chromosome 1 likely reflect the hitchhiking effect associated with OP insecticide selection.
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9

Waldbieser, Geoffrey C., Brian G. Bosworth, Danny J. Nonneman i William R. Wolters. "A Microsatellite-Based Genetic Linkage Map for Channel Catfish, Ictalurus punctatus". Genetics 158, nr 2 (1.06.2001): 727–34. http://dx.doi.org/10.1093/genetics/158.2.727.

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Abstract Microsatellite loci were identified in channel catfish gene sequences or random clones from a small insert genomic DNA library. Outbred populations of channel catfish contained an average of eight alleles per locus and an average heterozygosity of 0.70. A genetic linkage map of the channel catfish genome (N = 29) was constructed from two reference families. A total of 293 microsatellite loci were polymorphic in one or both families, with an average of 171 informative meioses per locus. Nineteen type I loci, 243 type II loci, and one EST were placed in 32 multipoint linkage groups covering 1958 cM. Nine more type II loci were contained in three two-point linkage groups covering 24.5 cM. Twenty-two type II loci remained unlinked. Multipoint linkage groups ranged in size from 11.9 to 110.5 cM with an average intermarker distance of 8.7 cM. Seven microsatellite loci were closely linked with the sex-determining locus. The microsatellite loci and genetic linkage map will increase the efficiency of selective breeding programs for channel catfish.
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10

Jin, Xiaoye, Xingru Zhang, Chunmei Shen, Yanfang Liu, Wei Cui, Chong Chen, Yuxin Guo i Bofeng Zhu. "A Highly Polymorphic Panel Consisting of Microhaplotypes and Compound Markers with the NGS and Its Forensic Efficiency Evaluations in Chinese Two Groups". Genes 11, nr 9 (1.09.2020): 1027. http://dx.doi.org/10.3390/genes11091027.

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Novel genetic markers like microhaplotypes and compound markers show promising potential in forensic research. Based on previously reported single nucleotide polymorphism (SNP) and insertion/deletion (InDel) polymorphism loci, 29 genetic markers including 22 microhaplotypes and seven compound markers were identified. Genetic distributions of the 29 loci in five continental populations, Kazak and Mongolian groups in China were investigated. We found that the expected heterozygosity values of these 29 loci were >0.4 in these populations, indicating these loci were relatively high polymorphisms. Population genetic analyses of five continental populations showed that five loci displayed relatively high genetic variations among these continental populations and could be useful markers for ancestry analysis. In summary, the 29 loci displayed relatively high genetic diversities in continental populations and Chinese two groups and could be informative loci for forensic research.
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Rozprawy doktorskie na temat "Genetic loci"

1

Chilakamarri, Sunita R. "Genetic differentiation in Alewife populations using microsatellite loci". Link to electronic thesis, 2005. http://www.wpi.edu/Pubs/ETD/Available/etd-053105-164623/.

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2

Nicholls, Felicity K. M. "Genetic analysis of the gene Additional sex combs and interacting loci". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29644.

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In order to recover new mutant alleles of the Polycomb group gene Additional sex combs (Asx), mutagenized chromosomes were screened over the putative Asx allele XT129. Thirteen new mutant strains that fail to complement XT129 were recovered. Unexpectedly, the thirteen strains sorted into four complementation groups. Recombination mapping suggests that each complementation group represents a separate locus. The largest group fails to complement a deletion of Asx and maps in the vicinity of 2-72, the published location of Asx. All new mutant strains enhance the phenotype of Polycomb mutant flies and are not allelic to any previously discovered second chromosome Polycomb group genes. Therefore, the new mutants may be considered putative new members of the Polycomb group. This study suggests that Asx belongs to a sub-group of genes displaying intergenic non-complementation.
Science, Faculty of
Zoology, Department of
Graduate
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3

Good, David Andrew, i n/a. "Genetic Loci for Paget's Disease of Bone". Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040319.125358.

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Paget's disease of the bone is a skeletal disorder of unknown cause. This disease is characterised by excessive and abnormal bone remodelling brought about by increased bone resorption followed by disorganised bone formation. Increased bone turnover results in a disorganised mosaic of woven and lamellar bone at affected skeletal sites. This produces bone that is expanded in size, less compact, more vascular, and more susceptible to deformity or fracture than normal bone. Symptoms of Paget's disease may include bone pain, bone deformity, excessive warmth over bone from hypervascularity, secondary arthritis, and a variety of neurologic complications caused in most instances by compression of the neural tissues adjacent to pagetic bone. Genetic factors play a role in the pathogenesis of Paget's disease but the molecular basis remains largely unknown. The identification of the molecular basis of Paget's disease is fundamental for an understanding of the cause of the disease, for identifying subjects at risk at a preclinical stage, and for the development of more effective preventive and therapeutic strategies for the management of the condition. With this in mind, the aim of this project is to identify genetic loci, in a large pedigree, that may harbour genes responsible for Paget's disease of bone. A large Australian family with evidence of Paget's disease was recruited for these studies (Chapter 3). This pedigree has characterised over 250 individuals, with 49 informative individuals affected with Paget's disease of bone, 31 of whom are available for genotypic analysis. The pattern of disease in these individuals is polystotic, with sites of involvement including the spine, pelvis, skull and femur. Although the affected individuals have a severe early-onset form of the disease, the clinical features of the pedigree suggest that the affected family members have Paget's disease and not familial expansile osteolysis (a disease with some similarities to Paget's disease), as our patients have extensive skull and axial skeletal involvement. The disease is inherited as an autosomal dominant trait in the pedigree with high penetrance by the sixth decade. Due to the large size of this family and multiple affected members, this pedigree is a unique resource for the detection of the susceptibility gene in Paget's disease. The first susceptibility loci for Paget's disease of bone have been mapped by other investigators to chromosome 6p21 (PDB1) and 18q21.1-q22 (PDB2) in different pedigrees. Linkage analysis of the Australian pedigree in these studies was performed with markers at PDB1: these data showed significant exclusion of linkage, with LOD scores < - 2 in this region (Chapter 4). Linkage analysis of microsatellite markers from the PDB2 region excluded linkage with this region also, with a 30 cM exclusion region (LOD score < -2.0) centred on D18S42 (Chapter 4). This locus on chromosome 18q21.1-q22 contains a serine protease (serpin) cluster with similarities to chromosome 6p21. Linkage analysis of this region also failed to provide evidence of linkage to this locus (Chapter 4). These data are consistent with genetic heterogeneity of Paget's disease of bone. A gene essential for osteoclast formation encoding receptor activator of nuclear factor-kB (RANK), TNFRSF11A, has been previously mapped to the PDB2 region. Mutations in the TNFRSF11A gene have been identified segregating in pedigrees with Familial Expansile Osteolysis and early onset familial Paget's disease, however, linkage studies and mutation screening have excluded the involvement of RANK in the majority of Paget's disease patients. For the Australian pedigree, mutation screening at the TNFRSF11A locus revealed no mutations segregating with affected individuals with Paget's disease (Chapter 4). Based on these findings, our hypothesis is that a novel susceptibility gene relevant to the pathogenesis of Paget's disease of bone lies elsewhere in the genome in the affected members of this pedigree; this gene should be identifiable using a microsatellite genome-wide scan followed by positional cloning. A genome-wide scan of the Australian pedigree was carried out, followed by fine mapping and multipoint analysis in regions of interest (Chapter 5). The peak 2-point LOD scores from the genome-wide scan were LOD = 2.75 at D7S507 and LOD = 1.76 at D18S70. Two additional regions were also considered for fine mapping: chromosome 19p11-q13.1 with a LOD of 1.58 and chromosome 5q35-qter with a LOD of 1.57. Multipoint and haplotype analysis of markers flanking D7S507 did not support linkage to this region (Chapter 5). Similarly, fine mapping of chromosome 19p11-q13.1 failed to support linkage to this region (Chapter 5). Linkage analysis with additional markers in the region on chromosome 5q35-qter revealed a peak multipoint LOD score of 6.77 (Chapter 5). A distinct haplotype was shown to segregate with all members of the family, except the offspring of III-5 and III-6. Haplotype analysis of markers flanking D18S70 demonstrated a haplotype segregating with Paget's disease in a large sub-pedigree (descendants of III-3 and III-4) (Chapter 5). This sub-pedigree had a significantly lower age at diagnosis than the rest of the pedigree (51.2 + 8.5 vs. 64.2 + 9.7 years, p = 0.0012). Linkage analysis of this sub-pedigree demonstrated a peak two-point LOD score of 4.23 at marker D18S1390 (q = 0.00), and a peak multipoint LOD score of 4.71, at marker D18S70. An implication of these data is that 18q23 harbours a novel modifier gene for reducing the age of onset of Paget's disease of bone. A number of candidate Paget's genes have previously been identified on chromosome 18q23, including the nuclear factor of activated T cells (NFATc1), membrane-associated guanylated kinase (MAGUK) and a zinc finger protein. Candidate gene sequencing of these genes in these studies has failed to identify mutations segregating with affected family members in the sub-pedigree linked to chromosome 18q23 (Chapter 6). More recently, a mutation in the gene encoding the ubiquitin-binding protein sequestosome 1 (SQSTM/p62) has been shown to segregate with affected members of Paget's disease families of French-Canadian origin. In this study, a single base pair deletion (1215delC) was identified as segregating with the majority of affected members in the pedigree (Chapter 6). This deletion introduces a stop codon at amino acid position 392 which potentially results in early termination of the protein and loss of the ubiquitin binding domain. The three affected members of the family that do not share the affected haplotype do not carry a mutation in the coding region of SQSTM/p62. Screening of affected members from 10 further Paget's disease families identified the previously reported P392L mutation in 2 (20%) families. No SQSTM1/p62 coding mutations have been found in the remaining 8 families or in 113 aged matched controls. In conclusion, this project has identified genetic loci and mutations that segregate with individuals affected with Paget's disease. Further investigation of the functional significance of the genetic changes at these loci is expected to lead to a better understanding of the molecular basis of this disease.
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4

Good, David Andrew. "Genetic Loci for Paget's Disease of Bone". Thesis, Griffith University, 2003. http://hdl.handle.net/10072/365759.

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Paget's disease of the bone is a skeletal disorder of unknown cause. This disease is characterised by excessive and abnormal bone remodelling brought about by increased bone resorption followed by disorganised bone formation. Increased bone turnover results in a disorganised mosaic of woven and lamellar bone at affected skeletal sites. This produces bone that is expanded in size, less compact, more vascular, and more susceptible to deformity or fracture than normal bone. Symptoms of Paget's disease may include bone pain, bone deformity, excessive warmth over bone from hypervascularity, secondary arthritis, and a variety of neurologic complications caused in most instances by compression of the neural tissues adjacent to pagetic bone. Genetic factors play a role in the pathogenesis of Paget's disease but the molecular basis remains largely unknown. The identification of the molecular basis of Paget's disease is fundamental for an understanding of the cause of the disease, for identifying subjects at risk at a preclinical stage, and for the development of more effective preventive and therapeutic strategies for the management of the condition. With this in mind, the aim of this project is to identify genetic loci, in a large pedigree, that may harbour genes responsible for Paget's disease of bone. A large Australian family with evidence of Paget's disease was recruited for these studies (Chapter 3). This pedigree has characterised over 250 individuals, with 49 informative individuals affected with Paget's disease of bone, 31 of whom are available for genotypic analysis. The pattern of disease in these individuals is polystotic, with sites of involvement including the spine, pelvis, skull and femur. Although the affected individuals have a severe early-onset form of the disease, the clinical features of the pedigree suggest that the affected family members have Paget's disease and not familial expansile osteolysis (a disease with some similarities to Paget's disease), as our patients have extensive skull and axial skeletal involvement. The disease is inherited as an autosomal dominant trait in the pedigree with high penetrance by the sixth decade. Due to the large size of this family and multiple affected members, this pedigree is a unique resource for the detection of the susceptibility gene in Paget's disease. The first susceptibility loci for Paget's disease of bone have been mapped by other investigators to chromosome 6p21 (PDB1) and 18q21.1-q22 (PDB2) in different pedigrees. Linkage analysis of the Australian pedigree in these studies was performed with markers at PDB1: these data showed significant exclusion of linkage, with LOD scores < - 2 in this region (Chapter 4). Linkage analysis of microsatellite markers from the PDB2 region excluded linkage with this region also, with a 30 cM exclusion region (LOD score < -2.0) centred on D18S42 (Chapter 4). This locus on chromosome 18q21.1-q22 contains a serine protease (serpin) cluster with similarities to chromosome 6p21. Linkage analysis of this region also failed to provide evidence of linkage to this locus (Chapter 4). These data are consistent with genetic heterogeneity of Paget's disease of bone. A gene essential for osteoclast formation encoding receptor activator of nuclear factor-kB (RANK), TNFRSF11A, has been previously mapped to the PDB2 region. Mutations in the TNFRSF11A gene have been identified segregating in pedigrees with Familial Expansile Osteolysis and early onset familial Paget's disease, however, linkage studies and mutation screening have excluded the involvement of RANK in the majority of Paget's disease patients. For the Australian pedigree, mutation screening at the TNFRSF11A locus revealed no mutations segregating with affected individuals with Paget's disease (Chapter 4). Based on these findings, our hypothesis is that a novel susceptibility gene relevant to the pathogenesis of Paget's disease of bone lies elsewhere in the genome in the affected members of this pedigree; this gene should be identifiable using a microsatellite genome-wide scan followed by positional cloning. A genome-wide scan of the Australian pedigree was carried out, followed by fine mapping and multipoint analysis in regions of interest (Chapter 5). The peak 2-point LOD scores from the genome-wide scan were LOD = 2.75 at D7S507 and LOD = 1.76 at D18S70. Two additional regions were also considered for fine mapping: chromosome 19p11-q13.1 with a LOD of 1.58 and chromosome 5q35-qter with a LOD of 1.57. Multipoint and haplotype analysis of markers flanking D7S507 did not support linkage to this region (Chapter 5). Similarly, fine mapping of chromosome 19p11-q13.1 failed to support linkage to this region (Chapter 5). Linkage analysis with additional markers in the region on chromosome 5q35-qter revealed a peak multipoint LOD score of 6.77 (Chapter 5). A distinct haplotype was shown to segregate with all members of the family, except the offspring of III-5 and III-6. Haplotype analysis of markers flanking D18S70 demonstrated a haplotype segregating with Paget's disease in a large sub-pedigree (descendants of III-3 and III-4) (Chapter 5). This sub-pedigree had a significantly lower age at diagnosis than the rest of the pedigree (51.2 + 8.5 vs. 64.2 + 9.7 years, p = 0.0012). Linkage analysis of this sub-pedigree demonstrated a peak two-point LOD score of 4.23 at marker D18S1390 (q = 0.00), and a peak multipoint LOD score of 4.71, at marker D18S70. An implication of these data is that 18q23 harbours a novel modifier gene for reducing the age of onset of Paget's disease of bone. A number of candidate Paget's genes have previously been identified on chromosome 18q23, including the nuclear factor of activated T cells (NFATc1), membrane-associated guanylated kinase (MAGUK) and a zinc finger protein. Candidate gene sequencing of these genes in these studies has failed to identify mutations segregating with affected family members in the sub-pedigree linked to chromosome 18q23 (Chapter 6). More recently, a mutation in the gene encoding the ubiquitin-binding protein sequestosome 1 (SQSTM/p62) has been shown to segregate with affected members of Paget's disease families of French-Canadian origin. In this study, a single base pair deletion (1215delC) was identified as segregating with the majority of affected members in the pedigree (Chapter 6). This deletion introduces a stop codon at amino acid position 392 which potentially results in early termination of the protein and loss of the ubiquitin binding domain. The three affected members of the family that do not share the affected haplotype do not carry a mutation in the coding region of SQSTM/p62. Screening of affected members from 10 further Paget's disease families identified the previously reported P392L mutation in 2 (20%) families. No SQSTM1/p62 coding mutations have been found in the remaining 8 families or in 113 aged matched controls. In conclusion, this project has identified genetic loci and mutations that segregate with individuals affected with Paget's disease. Further investigation of the functional significance of the genetic changes at these loci is expected to lead to a better understanding of the molecular basis of this disease.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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5

Roberts, Simon Benedict. "Investigating new genetic susceptibility loci in osteoarthritis". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28982.

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Primary osteoarthritis (OA) is a late-onset, degenerative condition of synovial joints, and is the major cause of pain and disability in older persons. OA represents a significant disease burden and focus of research, especially as no disease-modifying therapies exist to manage the condition. The genetic influence to OA is complex and polygenic. The arcOGEN study, the most powerful genome-wide association study yet to investigate OA in humans, identified the 9q33.1 locus to be significantly associated with hip OA in females. TRIM32 lies within the 9q33.1 susceptibility locus and may have strong biological relevance to OA; it encodes a protein with E3 ubiquitin ligase activity. Sanger sequencing of TRIM32 in the youngest 500 female patients with hip OA from the arcOGEN study was performed to identify rare variants in TRIM32 that are associated with OA of the hip in females. Polymorphisms were identified in the proximal promoter, and 3’untranslated regions (3’UTR) of TRIM32 that are disproportionately represented in female patients with hip OA, compared to the control population. In vitro studies identified expression of TRIM32 in human femoral head cartilage; reduced expression of TRIM32 was also demonstrated in femoral head primary articular chondrocytes from patients with hip OA compared to control patients. Trim32 knockout resulted in increased aggrecanolysis in murine femoral head explants. Murine chondrocytes deficient in Trim32 also exhibited increased expression of markers of a mature chondrocyte phenotype in response to anabolic cytokine stimulation, and increased expression of markers of a hypertrophic chondrocyte phenotype upon catabolic cytokine stimulation. In vivo studies of joint degeneration in Trim32 knockout mice demonstrated increased cartilage degradation and tibial epiphyseal bone changes after surgically induced knee joint instability, compared to wild-type mice. Increased cartilage degradation and medial knee subchondral bone changes were also identified upon ageing of Trim32 knockout mice. These results further implicate TRIM32 in the genetic predisposition to OA, and indicate a role for TRIM32 in the joint degeneration evident in OA. These results support the further study of TRIM32 in the pathophysiology of OA and development of novel therapeutic strategies to manage OA.
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6

Ahmed, Helal Uddin. "Mapping stress tolerance genetic loci in Arabidopsis thaliana". Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246628.

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Oakenfull, Elizabeth Ann. "A molecular genetic study of equid #alpha#-globin loci". Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317915.

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Mavridou, Annoula. "Genetic loci of Rhizobium leguminosarum affecting nod gene expression". Thesis, University of East Anglia, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316102.

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King, Alistair Lawrence. "Studies to identify genetic susceptibility loci in coeliac disease". Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406682.

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10

Rask-Andersen, Mathias. "Obesity Genetics : Functional Aspects of Four Genetic Loci Associated with Obesity and Body Mass". Doctoral thesis, Uppsala universitet, Funktionell farmakologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-204449.

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Obesity is a complex disorder which has reached epidemic proportions in many parts of the world. Twin studies have demonstrated a high heritability for obesity. The subsequent appli-cation of genome wide association studies (GWAS) in the last decade have identified at least 32 genetic loci associated with body mass and obesity. Despite these great advances, these loci are almost exclusively completely naïve in a functional context. Genetic variations within the gene encoding the fat mass and obesity associated gene (FTO) are the strongest and most consistently observed genetic variants associated with obesity and body mass throughout various studied populations from all parts of the world. The identification of association of FTO with obesity has spurred immense interest in the function of the FTO protein and the functional consequences of its variants. However, the implications of genetic variants at other genetic loci on protein molecular function and body mass development remain undetermined. This thesis aims to examine more closely four of the genetic loci associated with obesity; in proximity of, or associated with: FTO, TMEM18, MAP2K5 and STK33, in two cohorts of children of European descent: a case-control of clinically obese children and normal weight controls from the Stockholm area; and a cross sectional cohort of Greek children. These smaller cohorts allow for studies of more specific effects of genetic variants as individuals in these cohorts can be more carefully studied. TMEM18 gene expression was also studied in the rat-brain where a positive correlation was observed between the body weight of the animal and TMEM18 expression. We also employed next generation sequencing to more carefully study obesity-associated genetic loci related to FTO and TMEM18. We utilized a novel strategy in this project to study genetic variation in the entire FTO- and TMEM18 genes, as well as in the GWAS-identified BMI-associated loci located downstream from TMEM18. This analysis was performed on a case-control cohort of Swedish children (n = ~1000). Through this analysis, we were able to observe genetic variants within intron 1 of the FTO gene to be the main genetic variants asso-ciated with obesity at this locus. We also observed, for the first time, obesity-associated genetic variants within the gene encoding TMEM18. To analyze the potential functional context of FTO we used an in silico approach, utilizing public information databases on mRNA co-expression and protein-protein interaction. Based on our findings, we speculate on a wider functional role of FTO in extracellular ligand-induced neuronal plasticity, possibly via interaction or modulation of the BDNF/NTRK2 signaling pathway.
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Książki na temat "Genetic loci"

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Mavridou, Annoula. Genetic loci of Rhizobium leguminosarum affecting nod gene expression. Norwich: University of East Anglia, 1992.

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Population genetics of multiple loci. Chichester: Wiley, 2000.

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Weller, Joel Ira. Quantitative trait loci analysis in animals. Wyd. 2. Cambridge, MA: CABI North American Office, 2009.

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Weller, Joel Ira. Quantitative trait loci analysis in animals. Oxon, UK: CABI Pub., 2001.

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J, Camp Nicola, i Cox Angela 1961-, red. Quantitative trait loci: Methods and protocols. Totowa, N.J: Humana Press, 2002.

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Lantbruksuniversitet, Sveriges, red. Genome analysis of quantitative trait loci in the pig. Uppsala: Sveriges Lantbruksuniversitet, 1997.

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Miller, James R. X-linked traits: A catalog of loci in nonhuman mammals. Cambridge: Cambridge University Press, 1990.

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Saunak, Sen, i SpringerLink (Online service), red. A Guide to QTL Mapping with R/qtl. New York, NY: Springer-Verlag New York, 2009.

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Sepúlveda, Juan Ginés de. Io. Genesii Sepulvedae Cordubensis artium et sacrae theologiae doctor historicus Caesareus: Epistolarum libri septem in quibus cum alia multa quae legantur dignissima tradunter, tum varii loci graviorum doctrinarum eruditissime et elegantissime tractantur. Monachii et Lipsiae: in aedibus K.G. Saur, 2003.

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Sandler, Corey. Official Sega Genesis and Game Gear strategies, 3RD Edition. New York: Bantam Books, 1992.

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Części książek na temat "Genetic loci"

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Oestergaard, Mikkel Z., i Paul Pharoah. "Common Genetic Susceptibility Loci". W Breast Cancer Epidemiology, 301–20. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0685-4_14.

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Cardon, Lon R. "Quantitative Trait Loci". W Behavior Genetic Approaches in Behavioral Medicine, 237–50. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4757-9377-2_13.

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Millán, T., E. Madrid, P. Castro, J. Gil i J. Rubio. "Genetic Mapping and Quantitative Trait Loci". W Compendium of Plant Genomes, 83–106. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66117-9_8.

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Correia, César, Nuno Sepúlveda i Carlos Daniel Paulino. "Bayesian Genetic Mapping of Binary Trait Loci". W Advances in Regression, Survival Analysis, Extreme Values, Markov Processes and Other Statistical Applications, 139–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-34904-1_14.

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Baldoni, Luciana, Bouchaib Khadari i Raul De La Rosa. "Genetic Mapping and Detection of Quantitative Trait Loci". W Compendium of Plant Genomes, 65–74. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-48887-5_5.

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Epplen, Jörg T. "Simple Repeat Loci as Tools for Genetic Identification". W Ancient DNA, 13–30. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-4318-2_2.

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Chang, Bo. "Determination of Genomic Locations of Target Genetic Loci". W Gene Discovery for Disease Models, 111–38. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9780470933947.ch7.

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Semeiks, J. R., L. R. Grate i I. S. Mian. "Networks of genetic loci and the scientific literature". W Unifying Themes in Complex Systems, 296–303. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17635-7_36.

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Wilting, A., U. Hintzen, M. O. Völker i J. Bertrams. "Population genetic studies of six hypervariable DNA-Loci". W Advances in Forensic Haemogenetics, 252–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77324-2_77.

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Miao, Jiacheng, i Qiongshi Lu. "Identifying Genetic Loci Associated with Complex Trait Variability". W Springer Handbooks of Computational Statistics, 257–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65902-1_13.

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Streszczenia konferencji na temat "Genetic loci"

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Prokhorova, E. E., i R. R. Usmanova. "GENETIC POLYMORPHISM OF SNAILS SUCCINEA PUTRIS (GASTROPODA, PULMONATA)". W V International Scientific Conference CONCEPTUAL AND APPLIED ASPECTS OF INVERTEBRATE SCIENTIFIC RESEARCH AND BIOLOGICAL EDUCATION. Tomsk State University Press, 2020. http://dx.doi.org/10.17223/978-5-94621-931-0-2020-33.

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Genotypic diversity of snails Succinea putris L. (Linnaeus, 1758) collected in the north-west of Russia and in the Republic of Belarus was analysed. Homology between the nucleotide sequences of snails from different population made up 100% by the nucleotide sequence of ITS1-5.8S-ITS2 region of rDNA. Genetic variability based on mitochondrial markers was insignificant. Average genetic distances between samples made up 0,009 for СOI gene loci and 0.008 for CytB gene loci. Was found ten haplotypes of the mitochondrial gene CytB and nine haplotypes of the mitochondrial gene СOI. Perhaps the genetic homogeneity of snails S. putris found in the study explains a low variability of their parasites, trematodes from the genus Leucochloridium.
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Liu, Yang, Xiaojun Bai i Xiaofeng Kang. "Analysis and Study of the Correlation of Genetic Loci". W 2016 6th International Conference on Mechatronics, Computer and Education Informationization (MCEI 2016). Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/mcei-16.2016.237.

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Kramer, Patricia, Shawn K. Westaway, Martin Zwick i Stephen Shervais. "Reconstructability analysis of genetic loci associated with Alzheimer disease". W 2012 Joint 6th Intl. Conference on Soft Computing and Intelligent Systems (SCIS) and 13th Intl. Symposium on Advanced Intelligent Systems (ISIS). IEEE, 2012. http://dx.doi.org/10.1109/scis-isis.2012.6505196.

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Ilyasov, R. A., A. G. Nikolenko i H. W. Kwon. "GENETIC IMPROVEMENT OF HONEY BEES FOR KEEPING IN EXTREMAL CLIMATIC CONDITIONS". W V International Scientific Conference CONCEPTUAL AND APPLIED ASPECTS OF INVERTEBRATE SCIENTIFIC RESEARCH AND BIOLOGICAL EDUCATION. Tomsk State University Press, 2020. http://dx.doi.org/10.17223/978-5-94621-931-0-2020-55.

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Genetic improvement of honey bee populations based on molecular genetics features is faster and precision in comparison with morphometry and behavior-based methods. We developed the method based on nine nuclear microsatellite loci that allow a selection of most adaptive honey bee colonies by genetically defined features. Our study the heterozygosity of the dark European bee A. m. mellifera inhabiting the extremely cold region of the Ural Mountains to provide a marker-assisted selection for revealing the high adapted to extremely cold climate honey bee population can be applied for markerassisted selection of honey bees adapted to beekeeping in extremal climatic conditions.
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Johnatty, Sharon E., Jonathan Tyrer, Jonathan Beesley, Bo Gao, Yi Lu, Stuart MacGregor, Anna deFazio, Paul Pharoah, Ellen Goode i Georgia Chenevix-Trench. "Abstract 3286: Identification of genetic loci associated with ovarian cancer prognosis". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3286.

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Lu, Hong, i Lu Lu. "Expression quantitative trait loci and genetic regulatory network analysis of Fbn1". W INTERNATIONAL SYMPOSIUM ON THE FRONTIERS OF BIOTECHNOLOGY AND BIOENGINEERING (FBB 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5110812.

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Herrera Luis, E., V. E. Ortega, E. J. Ampleford, Y. Y. Sio, R. Granell, E. De Roos, N. Terzikhan i in. "Multi-ancestral meta-analysis yields novel genetic loci for asthma exacerbations". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.685.

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Saferali, A., W. Kim, J. H. Yun, M. Stav, R. Chase, M. H. Cho, P. Castaldi, C. P. Hersh, Z. Xu i Trans-Omics for Precision Medicine (TOPMed). "Overlap Between COPD Genetic Association Results and Transcriptional Quantitative Trait Loci". W American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4270.

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"Genetic loci for grain protein and gluten content in Russian spring wheat varieties". W Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Novosibirsk ICG SB RAS 2021, 2021. http://dx.doi.org/10.18699/plantgen2021-124.

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Wain, Louise, Mesut Erzurumluoglu, Carl Melbourne, Dany Doiron, Kees De Hoogh, Martin Tobin i Anna Hansell. "Interaction with air pollution exposure for genetic loci associated with lung function". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5395.

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Raporty organizacyjne na temat "Genetic loci"

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Gall, Graham A. E., Gideon Hulata, Eric M. Hallerman, Bernard May i Umiel Nakdimon. Creating and Characterizing Genetic Variation in Tilapia through the Creation of an Artificial Center of Origin. United States Department of Agriculture, luty 2000. http://dx.doi.org/10.32747/2000.7574344.bard.

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Five stocks of tilapia [oreochromis niloticus (on), red O. niloticus (ROn), O. aureus (Oa), O. mossambicus (Om), and Sarotherodon galilaeus (Sg)] were used to produce two-way (F1), three-way (3WC) and four-way crosses (4WC). Three 4WC groups, containing equal representation of all four species, formed the base population for a new synthetic stock, called an "artificial center of origin" (ACO). Four genomic maps were created using microsatellite and AFLP markers, two from a 3WC family [Om female and (Oa x ROn) male] and two from a 4WC family [(Om x Oas) females and (Sg x On) male]. Sixty-two loci segregating from the female parent of the 3WC mapped to 14 linkage groups while 214 loci from the male parent mapped to 24 linkage groups. Similarly, 131 loci segregating from the female parent of the 4WC mapped to 26 linkage groups and 118 loci from the male parent mapped to 25 linkage groups. Preliminary screening of an F2 and a 4WC family identified a number of loci associated with cold tolerance and body weight. These loci were clustered in a few linkage groups, suggesting they may be indicative of quantitative trait loci.
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Reisch, Bruce, Pinhas Spiegel-Roy, Norman Weeden, Gozal Ben-Hayyim i Jacques Beckmann. Genetic Analysis in vitis Using Molecular Markers. United States Department of Agriculture, kwiecień 1995. http://dx.doi.org/10.32747/1995.7613014.bard.

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Genetic analysis and mapping in grapes has been difficult because of the long generation period and paucity of genetic markers. In the present work, chromosome linkage maps were developed with RAPD, RFLP and isozyme loci in interspecific hybrid cultivars, and RAPD markers were produced in a V. vinifera population. In three cultivars, there were 19 linkage groups as expected for a species with 38 somatic chromosomes. These maps were used to locate chromosome regions with linkages to important genes, including those influencing powdery mildew and botrytis bunch rot resistance; flower sex; and berry shape. In V. vinifera, the occurrence of specific markers was correlated with seedlessness, muscat flavor and fruit color. Polymorphic RAPD bands included single copy as well as repetitive DNA. Mapping procedures were improved by optimizing PCR parameters with grape DNA; by the development of an efficient DNA extraction protocol; and with the use of long (17- to 24-mer) primers which amplify more polymorphic loci per primer. DNA fingerprint analysis with RAPD markers indicated that vinifera cultivars could be separated readily with RAPD profiles. Pinot gris, thought to be a sort of Pinot noir, differed by 12 bands from Pinot noir. This suggests that while Pinot gris may be related to Pinot noir, it is not likely to be a clone. The techniques developed in this project are now being further refined to use marker-assisted selection in breeding programs for the early selection of elite seedlings. Furthermore, the stage has been set for future attempts to clone genes from grapes based upon map locations.
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Guy, Charles, Gozal Ben-Hayyim, Gloria Moore, Doron Holland i Yuval Eshdat. Common Mechanisms of Response to the Stresses of High Salinity and Low Temperature and Genetic Mapping of Stress Tolerance Loci in Citrus. United States Department of Agriculture, maj 1995. http://dx.doi.org/10.32747/1995.7613013.bard.

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The objectives that were outlined in our original proposal have largely been achieved or will be so by the end of the project in February 1995 with one exception; that of mapping cold tolerance loci based on the segregation of tolerance in the BC1 progeny population. Briefly, our goals were to 1) construct a densely populated linkage map of the citrus genome: 2) map loci important in cold and/or salt stress tolerance; and 3) characterize the expression of genes responsive to cold land salt stress. As can be seen by the preceding listing of accomplishments, our original objectives A and B have been realized, objective C has been partially tested, objective D has been completed, and work on objectives E and F will be completed by the end of 1995. Although we have yet to map any loci that contribute to an ability of citrus to maintain growth when irrigated with saline water, our very encouraging results from the 1993 experiment provides us with considerable hope that 1994's much more comprehensive and better controlled experiment will yield the desired results once the data has been fully analyzed. Part of our optimism derives from the findings that loci for growth are closely linked with loci associated with foliar Cl- and Na+ accumulation patterns under non-salinization conditions. In the 1994 experiment, if ion exclusion or sequestration traits are segregating in the population, the experimental design will permit their resolution. Our fortunes with respect to cold tolerance is another situation. In three attempts to quantitatively characterize cold tolerance as an LT50, the results have been too variable and the incremental differences between sensitive and tolerant too small to use for mapping. To adequately determine the LT50 requires many plants, many more than we have been able to generate in the time and space available by making cuttings from small greenhouse-grown stock plants. As it has turned out, with citrus, to prepare enough plants needed to be successful in this objective would have required extensive facilities for both growing and testing hardiness which simply were not available at University of Florida. The large populations necessary to overcome the variability we encountered was unanticipated and unforeseeable at the project's outset. In spite of the setbacks, this project, when it is finally complete will be exceedingly successful. Listing of Accomplishments During the funded interval we have accomplished the following objectives: Developed a reasonably high density linkage map for citrus - mapped the loci for two cold responsive genes that were cloned from Poncirus - mapped the loci for csa, the salt responsive gene for glutathione peroxidase, and ccr a circadian rhythm gene from citrus - identified loci that confer parental derived specific DNA methylation patterns in the Citrus X Poncirus cross - mapped 5 loci that determine shoot vigor - mapped 2 loci that influence leaf Na+ accumulation patterns under non-saline conditions in the BC1 population - mapped 3 loci that influence leaf Na+ accumulation paterns during salt sress - mapped 2 loci that control leaf Cl- accumulation patterns under non-saline conditions - mapped a locus that controls leaf Cl- accumulation patterns during salt stress Screened the BC1 population for growth reduction during salinization (controls and salinized), and cold tolerance - determined population variation for shoot/root ratio of Na+ and Cl- - determined levels for 12 inorganic nutrient elements in an effort to examine the influence of salinization on ion content with emphasis on foliar responses - collected data on ion distribution to reveal patterns of exclusion/sequestration/ accumulation - analyzed relationships between ion content and growth Characterization of gene expression in response to salt or cold stress - cloned the gene for the salt responsive protein csa, identified it as glutathione peroxidase, determined the potential target substrate from enzymatic studies - cloned two other genes responsive to salt stress, one for the citrus homologue of a Lea5, and the other for an "oleosin" like gene - cold regulated (cor) genes belonging to five hybridization classes were isolated from Poncirus, two belonged to the group 2 Lea superfamily of stress proteins, the others show no significant homology to other known sequences - the expression of csa during cold acclimation was examined, and the expression of some of the cor genes were examined in response to salt stress - the influence of salinization on cold tolerance has been examined with seedling populations - conducted protein blot studies for expression of cold stress proteins during salt stress and vice versa
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Zhang, Hongbin B., David J. Bonfil i Shahal Abbo. Genomics Tools for Legume Agronomic Gene Mapping and Cloning, and Genome Analysis: Chickpea as a Model. United States Department of Agriculture, marzec 2003. http://dx.doi.org/10.32747/2003.7586464.bard.

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The goals of this project were to develop essential genomic tools for modern chickpea genetics and genomics research, map the genes and quantitative traits of importance to chickpea production and generate DNA markers that are well-suited for enhanced chickpea germplasm analysis and breeding. To achieve these research goals, we proposed the following research objectives in this period of the project: 1) Develop an ordered BAC library with an average insert size of 150 - 200 kb (USA); 2) Develop 300 simple sequence repeat (SSR) markers with an aid of the BAC library (USA); 3) Develop SSR marker tags for Ascochyta response, flowering date and grain weight (USA); 4) Develop a molecular genetic map consisting of at least 200 SSR markers (Israel and USA); 5) Map genes and QTLs most important to chickpea production in the U.S. and Israel: Ascochyta response, flowering and seed set date, grain weight, and grain yield under extreme dryland conditions (Israel); and 6) Determine the genetic correlation between the above four traits (Israel). Chickpea is the third most important pulse crop in the world and ranks the first in the Middle East. Chickpea seeds are a good source of plant protein (12.4-31.5%) and carbohydrates (52.4-70.9%). Although it has been demonstrated in other major crops that the modern genetics and genomics research is essential to enhance our capacity for crop genetic improvement and breeding, little work was pursued in these research areas for chickpea. It was absent in resources, tools and infrastructure that are essential for chickpea genomics and modern genetics research. For instance, there were no large-insert BAC and BIBAC libraries, no sufficient and user- friendly DNA markers, and no intraspecific genetic map. Grain sizes, flowering time and Ascochyta response are three main constraints to chickpea production in drylands. Combination of large seeds, early flowering time and Ascochyta blight resistance is desirable and of significance for further genetic improvement of chickpea. However, it was unknown how many genes and/or loci contribute to each of the traits and what correlations occur among them, making breeders difficult to combine these desirable traits. In this period of the project, we developed the resources, tools and infrastructure that are essential for chickpea genomics and modern genetics research. In particular, we constructed the proposed large-insert BAC library and an additional plant-transformation-competent BIBAC library from an Israeli advanced chickpea cultivar, Hadas. The BAC library contains 30,720 clones and has an average insert size of 151 kb, equivalent to 6.3 x chickpea haploid genomes. The BIBAC library contains 18,432 clones and has an average insert size of 135 kb, equivalent to 3.4 x chickpea haploid genomes. The combined libraries contain 49,152 clones, equivalent to 10.7 x chickpea haploid genomes. We identified all SSR loci-containing clones from the chickpea BAC library, generated sequences for 536 SSR loci from a part of the SSR-containing BACs and developed 310 new SSR markers. From the new SSR markers and selected existing SSR markers, we developed a SSR marker-based molecular genetic map of the chickpea genome. The BAC and BIBAC libraries, SSR markers and the molecular genetic map have provided essential resources and tools for modern genetic and genomic analyses of the chickpea genome. Using the SSR markers and genetic map, we mapped the genes and loci for flowering time and Ascochyta responses; one major QTL and a few minor QTLs have been identified for Ascochyta response and one major QTL has been identified for flowering time. The genetic correlations between flowering time, grain weight and Ascochyta response have been established. These results have provided essential tools and knowledge for effective manipulation and enhanced breeding of the traits in chickpea.
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Ginzberg, Idit, i Walter De Jong. Molecular genetic and anatomical characterization of potato tuber skin appearance. United States Department of Agriculture, wrzesień 2008. http://dx.doi.org/10.32747/2008.7587733.bard.

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Potato (Solanum tuberosum L.) skin is composed of suberized phellem cells, the outer component of the tuber periderm. The focus of the proposed research was to apply genomic approaches to identify genes that control tuber skin appearance - smooth and shiny skin is highly preferred by the customers while russeted/netted skin potatoes are rejected. The breeding program (at Cornell University) seeks to develop smooth-skin varieties but has encountered frequent difficulties as inheritance of russeting involves complementary action by independently segregating genes, where a dominant allele at each locus is required for any degree of skin russeting. On the other hand, smooth-skin varieties frequently develop unsightly russeting in response to stress conditions, mainly high soil temperatures. Breeding programs in Israel aimed towards the improvement of heat tolerant varieties include skin quality as one of the desired characteristics. At the initiation of the present project it was unclear whether heat induced russeting and genetically inherited russeting share the same genes and biosynthesis pathways. Nevertheless, it has been suggested that russeting might result from increased periderm thickness, from strong cohesion between peridermal cells that prevents the outer layers from sloughing off, or from altered suberization processes in the skin. Hence, the original objectives were to conduct anatomical study of russet skin development, to isolate skin and russeting specific genes, to map the loci that determine the russet trait, and to compare with map locations the candidate russet specific genes, as well as to identify marker alleles that associated with russet loci. Anatomical studies suggested that russet may evolve from cracking at the outer layers of the skin, probably when skin development doesn’t meet the tuber expansion rate. Twodimensional gel electrophoresis and transcript profiling (cDNA chip, potato functional genomic project) indicated that in comparison to the parenchyma tissue, the skin is enriched with proteins/genes that are involved in the plant's responses to biotic and abiotic stresses and further expand the concept of the skin as a protective tissue containing an array of plantdefense components. The proteomes of skin from heat stressed tubers and native skin didn’t differ significantly, while transcript profiling indicated heat-related increase in three major functional groups: transcription factors, stress response and protein degradation. Exceptional was ACC synthase isogene with 4.6 fold increased level in the heat stressed skin. Russeting was mapped to two loci: rusB on chromosome 4 and rusC on chromosome 11; both required for russeting. No evidence was found for a third locus rusA that was previously proposed to be required for russeting. In an effort to find a link between the russeting character and the heat-induced russeting an attempt was made to map five genes that were found in the microarray experiment to be highly induced in the skin under heat stress in the segregating russet population. Only one gene was polymorphic; however it was localized to chromosome 2, so cannot correspond to rusB or rusC. Evaluation of AFLP markers tightly linked to rusB and rusC showed that these specific alleles are not associated with russeting in unrelated germplasm, and thus are not useful for MAS per se. To develop markers useful in applied breeding, it will be necessary to screen alleles of additional tightly linked loci, as well as to identify additional russet (heat-induced and/or native) related genes.
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Moore, Gloria A., Gozal Ben-Hayyim, Charles L. Guy i Doron Holland. Mapping Quantitative Trait Loci in the Woody Perennial Plant Genus Citrus. United States Department of Agriculture, maj 1995. http://dx.doi.org/10.32747/1995.7570565.bard.

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As is true for all crops, production of Citrus fruit is limited by traits whose characteristics are the products of many genes (i.e. cold hardiness). In order to modify these traits by marker aided selection or molecular genetic techniques, it is first necessary to map the relevant genes. Mapping of quantitative trait loci (QTLs) in perennial plants has been extremely difficult, requiring large numbers of mature plants. Production of suitable mapping populations has been inhibited by aspects of reproductive biology (e.g. incompatibility, apomixis) and delayed by juvenility. New approaches promise to overcome some of these obstacles. The overall objective of this project was to determine whether QTLs for environmental stress tolerance could be effectively mapped in the perennial crop Citrus, using an extensive linkage map consisting of various types of molecular markers. Specific objectives were to: 1) Produce a highly saturated genetic linkage map of Citrus by continuing to place molecular markers of several types on the map. 2) Exploiting recently developed technology and already characterized parental types, determine whether QTLs governing cold acclimation can be mapped using very young seedling populations. 3) Determine whether the same strategy can be transferred to a different situation by mapping QTLs influencing Na+ and C1- exclusion (likely components of salinity tolerance) in the already characterized cross and in new alternative crosses. 4) Construct a YAC library of the citrus genome for future mapping and cloning.
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Wisniewski, Michael E., Samir Droby, John L. Norelli, Noa Sela i Elena Levin. Genetic and transcriptomic analysis of postharvest decay resistance in Malus sieversii and the characterization of pathogenicity effectors in Penicillium expansum. United States Department of Agriculture, styczeń 2014. http://dx.doi.org/10.32747/2014.7600013.bard.

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Blue mold of apple caused by Penicilliumexpansumis a major postharvest disease. Selection for postharvest disease resistance in breeding programs has been ignored in favor of fruit quality traits such as size, color, taste, etc. The identification of postharvest disease resistance as a heritable trait would represent a significant accomplishment and has not been attempted in apple. Furthermore, insight into the biology of the pathogenicity of P. expansumin apple could provide new approaches to postharvest decay management. Hypothesis: Postharvest resistance of apple to P. expansumcan be mapped to specific genetic loci and significant quantitative-trait-loci (QTLs) can be identified that account for a major portion of the population variance. Susceptibility of apple fruit to P. expansumis dependent on the ability of the pathogen to produce LysM effectors that actively suppress primary and/or secondary resistance mechanisms in the fruit. Objectives: 1) Identify QTL(s) and molecular markers for blue mold resistance in GMAL4593 mapping population (‘Royal Gala’ X MalussieversiiPI613981), 2) Characterize the transcriptome of the host and pathogen (P. expansum) during the infection process 3) Determine the function of LysM genes in pathogenicity of P. expansum. Methods: A phenotypic evaluation of blue mold resistance in the GMAL4593 mapping population, conducted in several different years, will be used for QTL analysis (using MapQTL 6.0) to identify loci associated with blue mold resistance. Molecular markers will be developed for the resistance loci. Transcriptomic analysis by RNA-seq will be used to conduct a time course study of gene expression in resistant and susceptible apple GMAL4593 genotypes in response to P. expansum, as well as fungal responses to both genotypes. Candidate resistance genes identified in the transcriptomic study and or bioinformatic analysis will be positioned in the ‘Golden Delicious’ genome to identify markers that co-locate with the identified QTL(s). A functional analysis of LysM genes on pathogenicity will be conducted by eliminating or reducing the expression of individual effectors by heterologous recombination and silencing technologies. LysMeffector genes will also be expressed in a yeast expression system to study protein function. Expected Results: Identification of postharvest disease resistance QTLs and tightly-linked genetic markers. Increased knowledge of the role of effectors in blue mold pathogenic
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Weller, Joel, Harris Lewin, Micha Ron i George Wiggans. Detection and Mapping of Genes Affecting Traits of Economic Importance in Dairy Cattle with the Aid of Molecular Genetic Markers. United States Department of Agriculture, grudzień 1995. http://dx.doi.org/10.32747/1995.7613024.bard.

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Forty-seven poly-TG microsatellites were developed at the U of IL, and 11 genetic markers were developed at ARO, nine of which were poly-AGC microsatellites. Markers were typed on the reference families of CSIRO, Australia; GRANADA, Texas; and IRRF, Illinois, for chromosome assignment and linkage mapping. Nine North American al organizations contributed semen to the Dairy Bull DNA Repository (DBDR), which currently has 65,743 units from 3366 bulls. Semen was obtained for 31 out of 35 grandsires. Semen of 28 and 23 sons of two Israeli bulls was also collected. Eighteen grandsires were genotyped for 75 microsatellites. One thousand, three hundred and sixty-two sons with evaluation from 17 families were genotyped for 24 markers. Eleven thousand, six hundred and twenty sons genotypes were determined, of which 8,802 were informative. The genotype data was matched to the bulls' daughter yield deviations (DYD) for seven traits; milk, fat, and protein production; fat and protein percent; somatic cell concentration (SCS); and productive herd life. Seven loci had significant effects at p<0.05, but only two loci, TGLA263 and MGTG7, had significant effects at p<0.01, and the effect of TGLA263 on fat percentage was significant at p<0.0001. There was at least one significant effect for each of the seven traits analyzed.
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Weller, Joel I., Harris A. Lewin i Micha Ron. Determination of Allele Frequencies for Quantitative Trait Loci in Commercial Animal Populations. United States Department of Agriculture, luty 2005. http://dx.doi.org/10.32747/2005.7586473.bard.

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Individual loci affecting economic traits in dairy cattle (ETL) have been detected via linkage to genetic markers by application of the granddaughter design in the US population and the daughter design in the Israeli population. From these analyses it is not possible to determine allelic frequencies in the population at large, or whether the same alleles are segregating in different families. We proposed to answer this question by application of the "modified granddaughter design", in which granddaughters with a common maternal grandsire are both genotyped and analyzed for the economic traits. The objectives of the proposal were: 1) to fine map three segregating ETL previously detected by a daughter design analysis of the Israeli dairy cattle population; 2) to determine the effects of ETL alleles in different families relative to the population mean; 3) for each ETL, to determine the number of alleles and allele frequencies. The ETL on Bostaurusautosome (BT A) 6 chiefly affecting protein concentration was localized to a 4 cM chromosomal segment centered on the microsatellite BM143 by the daughter design. The modified granddaughter design was applied to a single family. The frequency of the allele increasing protein percent was estimated at 0.63+0.06. The hypothesis of equal allelic frequencies was rejected at p<0.05. Segregation of this ETL in the Israeli population was confirmed. The genes IBSP, SPP1, and LAP3 located adjacent to BM143 in the whole genome cattle- human comparative map were used as anchors for the human genome sequence and bovine BAC clones. Fifteen genes within 2 cM upstream of BM143 were located in the orthologous syntenic groups on HSA4q22 and HSA4p15. Only a single gene, SLIT2, was located within 2 cM downstream of BM143 in the orthologous HSA4p15 region. The order of these genes, as derived from physical mapping of BAC end sequences, was identical to the order within the orthologous syntenic groups on HSA4: FAM13A1, HERC3. CEB1, FLJ20637, PP2C-like, ABCG2, PKD2. SPP, MEP, IBSP, LAP3, EG1. KIAA1276, HCAPG, MLR1, BM143, and SLIT2. Four hundred and twenty AI bulls with genetic evaluations were genotyped for 12 SNPs identified in 10 of these genes, and for BM143. Seven SNPs displayed highly significant linkage disequilibrium effects on protein percentage (P<0.000l) with the greatest effect for SPP1. None of SNP genotypes for two sires heterozygous for the ETL, and six sires homozygous for the ETL completely corresponded to the causative mutation. The expression of SPP 1 and ABCG2 in the mammary gland corresponded to the lactation curve, as determined by microarray and QPCR assays, but not in the liver. Anti-sense SPP1 transgenic mice displayed abnormal mammary gland differentiation and milk secretion. Thus SPP 1 is a prime candidate gene for this ETL. We confirmed that DGAT1 is the ETL segregating on BTA 14 that chiefly effects fat concentration, and that the polymorphism is due to a missense mutation in an exon. Four hundred Israeli Holstein bulls were genotyped for this polymorphism, and the change in allelic frequency over the last 20 years was monitored.
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Hulata, Gideon, i Graham A. E. Gall. Breed Improvement of Tilapia: Selective Breeding for Cold Tolerance and for Growth Rate in Fresh and Saline Water. United States Department of Agriculture, listopad 2003. http://dx.doi.org/10.32747/2003.7586478.bard.

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The main objective of this project was to initiate a breeding program to produce cold-tolerant and salinity-tolerant synthetic breeds of tilapia, from a base population consisting of a four-species hybrid population created under an earlier BARD project. A secondary objective was to estimate genetic parameters for the traits growth rate under fresh- and salt-water and for cold tolerance. A third objective was to place quantitative trait loci that affect these traits of interest (e.g., growth rate in fresh-water, salt-water and cold tolerance) on the growing linkage map of primarily microsatellite loci. We have encountered fertility problems that were apparently the result of the complex genetic structure of this base population. The failure in producing the first generation of the breeding program has forced us to stop the intended breeding program. Thus, upon approval of BARD office, this objective was dropped and during the last year we have focused on the secondary objective of the original project during the third year of the project, but failed to perform the intended analysis to estimate genetic parameters for the traits of interest. We have succeeded, however, to strengthen the earlier identification of a QTL for cold tolerance by analyzing further segregating families. The results support the existence of a QTL for cold tolerance on linkage group 15, corresponding to UNH linkage group 23. The results also indicate a QTL for the same trait on linkage group 12, corresponding to UNH linkage group 4.
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