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Lena C. Hileman - One of the best experts on this subject based on the ideXlab platform.
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nectary size is a pollination syndrome trait in penstemon
New Phytologist, 2019Co-Authors: Amanda M Katzer, Carolyn A Wessinger, Lena C. HilemanAbstract:: Evolution of complex phenotypes depends on the adaptive importance of individual traits, and the developmental changes required to modify traits. Floral syndromes are complex adaptations to pollinators that include color, nectar, and shape variation. Hummingbird-adapted flowers have evolved a remarkable number of times from bee-adapted ancestors in Penstemon, and previous work demonstrates that color over shape better distinguishes bee from hummingbird syndromes. Here, we examined the relative importance of nectar volume and nectary development in defining Penstemon pollination syndromes. We tested the evolutionary association of nectar volume and nectary area with pollination syndrome aCross 19 Penstemon species. In selected species, we assessed cellular-level processes shaping nectary size. Within a segregating population from an intersyndrome Cross, we assessed trait correlations between nectar volume, nectary area, and the size of stamens on which nectaries develop. Nectar volume and nectary area displayed an evolutionary association with pollination syndrome. These traits were correlated within a Genetic Cross, suggesting a mechanistic link. Nectary area evolution involves parallel processes of cell expansion and proliferation. Our results demonstrate that changes to nectary patterning are an important contributor to pollination syndrome diversity and provide further evidence that repeated origins of hummingbird adaptation involve parallel developmental processes in Penstemon.
Edward K Wakeland - One of the best experts on this subject based on the ideXlab platform.
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production of congenic mouse strains carrying genomic intervals containing sle susceptibility genes derived from the sle prone nzm2410 strain
Mammalian Genome, 1996Co-Authors: Laurence Morel, Ying Yu, Kim R M Blenman, R A Caldwell, Edward K WakelandAbstract:Systemic lupus erythematosus is inherited as a complex polygenic trait. Four genomic intervals containing major SLE-susceptibility loci were previously identified by interval mapping in the NZM2410 mouse model. In this paper, we utilized a marker-assisted selection protocol to produce four congenic mouse strains, each carrying an NZM2410-derived SLE-susceptibility interval on a C57BL/6-resistant background. Each strain carries only one susceptibility allele derived from this polygenic model and consequently can be used to characterize the specific component phenotypes contributed by individual SLE-susceptibility genes. We illustrate the efficacy of this approach with phenotypic data for one of our congenic strains, B6.NZMH2Z. Our results indicate that this single genomic interval from Chromosome (Chr) 17 of NZM2410 can mediate increased levels of IgG autoantibodies specific for chromatin and that, similar to results obtained in our original Genetic Cross, B6.NZMH2z/b heterozygotes are more prone than B6.NZMH2z homozygotes to the development of humoral autoimmunity to nuclear antigens. These results illustrate the feasibility of using congenic strains to dissect the complex pathogenic mechanisms that mediate polygenic SLE. These congenic strains will be valuable tools in the Genetic analysis of SLE susceptibility. In future studies, these congenic strains will be interbred to produce bi- and tri-congenic strains in order to assess the role of Genetic interactions in the expression of specific components of SLE pathogenesis. They will also be instrumental to the positional cloning and identification of the genes responsible for SLE susceptibility, via the production of congenic recombinants.
S Mayama - One of the best experts on this subject based on the ideXlab platform.
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analysis of host species specificity of magnaporthe grisea toward wheat using a Genetic Cross between isolates from wheat and foxtail millet
Phytopathology, 2000Co-Authors: Jiro Murakami, Yukio Tosa, Hitoshi Nakayashiki, Izumi Chuma, T Kataoka, R Tomita, J Kawasaki, Y Sesumi, Motoaki Kusaba, S MayamaAbstract:ABSTRACT A Genetic Cross was performed between a Setaria isolate (pathogenic on foxtail millet) and a Triticum isolate (pathogenic on wheat) of Magnaporthe grisea to elucidate Genetic mechanisms of its specific parasitism toward wheat. A total of 80 F1 progenies were obtained from 10 mature asci containing 8 ascospores. Lesions on wheat leaves produced by the F1 progenies were classified into four types, which segregated in a 1:1:1:1 ratio. This result suggested that the pathogenicity of the F1 population on wheat was controlled by two genes located at different loci. This idea was supported by backCross analyses. We designated these loci as Pwt1 and Pwt2. Cytological analyses revealed that Pwt1 and Pwt2 were mainly associated with the hypersensitive reaction and papilla formation, respectively.
Louis Bernier - One of the best experts on this subject based on the ideXlab platform.
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localization of a pathogenicity gene in ophiostoma novo ulmi and evidence that it may be introgressed from o ulmi
Molecular Plant-microbe Interactions, 1999Co-Authors: Abdelali Ettouil, C M Brasier, Louis BernierAbstract:Ophiostoma novo-ulmi, the principal agent of Dutch elm disease, has recently replaced another species of Dutch elm disease pathogen, O. ulmi, aCross much of the Northern Hemisphere. Field inoculations of the moderately resistant elms Ulmus procera and Ulmus × Commelin were carried out with progeny of a Genetic Cross between AST27, a Eurasian (EAN) O. novo-ulmi isolate with an unusually low level of pathogenicity, and H327, a highly aggressive EAN isolate. These confirmed the results of a previous study that indicated that the difference in phenotype was controlled by a single nuclear gene. This pathogenicity gene, designated here Pat1, is the first putative pathogenicity gene to be identified in O. novo-ulmi. In a bulked segregant analysis, involving 80 random primers, 10 RAPD (random amplified polymorphic DNA) markers were identified linked to Pat1. Linkage distances between these markers and Pat1 were confirmed by Genetic analysis of all individual progeny. Five RAPD amplicons identified in AST27 were O...
Thomas E. Wellems - One of the best experts on this subject based on the ideXlab platform.
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Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum
Nature Chemical Biology, 2009Co-Authors: Jing Yuan, Thomas E. Wellems, Hongying Jiang, Karen Hayton, David A Fidock, Ronald L Johnson, Ruili Huang, Jennifer Wichterman, James Inglese, Christopher P AustinAbstract:Studies of gene function and molecular mechanisms in Plasmodium falciparum are hampered by difficulties in characterizing and measuring phenotypic differences between individual parasites. We screened seven parasite lines for differences in responses to 1,279 bioactive chemicals. Hundreds of compounds were active in inhibiting parasite growth; 607 differential chemical phenotypes, defined as pairwise IC_50 differences of fivefold or more between parasite lines, were cataloged. We mapped major determinants for three differential chemical phenotypes between the parents of a Genetic Cross, and we identified target genes by fine mapping and testing the responses of parasites in which candidate genes were Genetically replaced with mutant alleles. Differential sensitivity to dihydroergotamine methanesulfonate ( 1 ), a serotonin receptor antagonist, was mapped to a gene encoding the homolog of human P-glycoprotein (PfPgh-1). This study identifies new leads for antimalarial drugs and demonstrates the utility of a high-throughput chemical genomic strategy for studying malaria traits.
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EBL-1, a putative erythrocyte binding protein of Plasmodium falciparum, maps within a favored linkage group in two Genetic Crosses.
Molecular and biochemical parasitology, 2000Co-Authors: David S Peterson, Thomas E. WellemsAbstract:The Duffy binding-like (DBL) superfamily of Plasmodium falciparum encompasses genes which encode ligands for host cell receptors. This superfamily includes two distinct groups of genes, the var genes which encode antigenically variant cytoadherence proteins (PfEMP1), and the eba-175 gene which encodes a glycophorin A binding protein involved in erythrocyte invasion. Here we describe another DBL superfamily member related to eba-175, the ebl-1 gene. Like the eba-175 gene, ebl-1 is a single copy gene encoding DBL domains that have sequences and an overall arrangement distinct from var genes. The inheritance of ebl-1 was found to be strongly favored in two Genetic Crosses in which one parental clone lacked a chromosome segment carrying the gene. A proliferation phenotype has been previously linked to the same chromosome segment in the first Genetic Cross. These results suggest that ebl-1 and eba-175 are related members of a multigene family involved in the invasion of erythrocytes by P. falciparum.
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a Genetic map and recombination parameters of the human malaria parasite plasmodium falciparum
Science, 1999Co-Authors: Xinzhuan Su, Michael T. Ferdig, Yaming Huang, Chuong Q Huynh, John C Wootton, Thomas E. WellemsAbstract:Genetic investigations of malaria require a genome-wide, high-resolution linkage map of Plasmodium falciparum. A Genetic Cross was used to construct such a map from 901 markers that fall into 14 inferred linkage groups corresponding to the 14 nuclear chromosomes. Meiotic Crossover activity in the genome proved high (17 kilobases per centimorgan) and notably uniform over chromosome length. Gene conversion events and spontaneous microsatellite length changes were evident in the inheritance data. The markers, map, and recombination parameters are facilitating genome sequence assembly, localization of determinants for such traits as virulence and drug resistance, and Genetic studies of parasite field populations.
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An RFLP map of the Plasmodium falciparum genome, recombination rates and favored linkage groups in a Genetic Cross.
Molecular and biochemical parasitology, 1992Co-Authors: Annie Walker-jonah, Stephen A. Dolan, Robert W. Gwadz, Lindsey J. Panton, Thomas E. WellemsAbstract:We report a Genetic linkage map of the Plasmodium falciparum genome, using the inheritance patterns of nearly 90 RFLP markers in a Genetic Cross. Markers were assigned to polymorphic loci on all 14 nuclear chromosomes. Genetic recombination between parental markers was detected in each of the progeny, indicating that progeny from Cross-fertilization events were favored over progeny from self-fertilization of either parent alone. Inheritance patterns among the markers suggested that certain parental linkage groups on chromosomes 2, 3, 12 and 13 were favored in the Cross. Recombination frequencies on five chromosomes indicated an approximate map unit size of 15-30 kb per centiMorgan for P. falciparum.
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chloroquine resistance not linked to mdr like genes in a plasmodium falciparum Cross
Nature, 1990Co-Authors: Thomas E. Wellems, Robert W. Gwadz, L J Panton, Ilya Y Gluzman, V Do E Rosario, A Walkerjonah, Donald J KrogstadAbstract:CHLOROQUINE is thought to act against falciparum malaria by accumulating in the acid vesicles of the parasite and interfering with their function1–4. Parasites resistant to chloroquine expel the drug rapidly in an unaltered form, thereby reducing levels of accumulation in the vesicles5. The discovery that verapamil partially reverses chloroquine resistance in vitro6 led to the proposal that efflux may involve an ATP-driven P-glycoprotein pump similar to that in mammalian multidrug-resistant (mdr) tumor cell lines. Indeed, Plasmodium falciparum contains at least two mdr-like genes7,8, one of which has been suggested to confer the chloroquine resistant (CQR) phenotype7,9,10. To determine if either of these genes is linked to chloroquine resistance, we performed a Genetic Cross between CQR and chloroquine-susceptible (CQS) clones of P. falciparum. Examination of 16 independent recombinant progeny indicated that the rapid efflux phenotype is controlled by a single gene or a closely linked group of genes. But, there was no linkage between the rapid efflux, CQR phenotype and either of the mdr-like P. falciparum genes or amplification of those genes. These data indicate that the Genetic locus governing chloroquine efflux and resistance is independent of the known mdr-like genes.