The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Donald W. Paty - One of the best experts on this subject based on the ideXlab platform.
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study of alleles of the second complement component c2 on canadian hla Haplotypes
Tissue Antigens, 2008Co-Authors: W. H. Marshall, John M Barnard, Nadir R Farid, R Grandy, Bodil Larsen, Ronald Payne, Verna M Skanes, David N. Churchill, George Cornell Ebers, Donald W. PatyAbstract:Typing for genetic variation in the second complement component C2 was performed on sera from HLA Haplotyped Canadian families. Part of the data has been studied and analysed as a population; in addition there is a further random collection of Haplotypes bearing the C2*2 allele. In the population data there were 444 separate Haplotypes from unrelated parents or other founders: 4.7% of the Haplotypes carried the uncommon allele C2*2; one Haplotype carried the rare C2*3. Study of C2 2–1 heterozygotes in the population data revealed 59 Haplotypes which carried the common C2*1 allele and one which carried a deficiency allele C2*0. The remaining Haplotypes carried either C2* 1 or else an undetectable C2*0 allele. In the entire data there were 281 meioses informative for C2. The only recombinant between HLA-B and C2 showed the C2 locus to be on the DR side of the B locus. Strong allelic association between C2 *2 and Bw22 and less strong association between C2 *2 and B15 suggested the possibility of two ancestral C2 mutants. Examination of other markers on these and subsequently collected Haplotypes do not conflict with this idea since the B15 Haplotypes mostly carry C4A *4, C4B*2 whilst the Bw22 Haplotypes mostly carry C4A*4, C4B*4. The alternative idea, that there was one original mutant which crossed over from a B15 to a Bw22 Haplotype or vice versa is not excluded, however. Since approximate equilibrium has been reached between Bw22 and the HLA-A locus alleles on these C2*2 bearing Haplotypes, we conclude that this mutation is at least 5000 years old. Other Haplotypes carrying C2*2 are assumed to be ancestral recombinants; if this is true, the C2 locus map position between HLA-B and HLA-DR is confirmed. Study of C2 mutation may provide a model for understanding the genetics of some disease susceptibility genes in the HLA region.
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study of alleles of the second complement component c2 on canadian hla Haplotypes
Tissue Antigens, 2008Co-Authors: W. H. Marshall, John M Barnard, Nadir R Farid, R Grandy, Bodil Larsen, Ronald Payne, Verna M Skanes, David N. Churchill, George Cornell Ebers, Donald W. PatyAbstract:Typing for genetic variation in the second complement component C2 was performed on sera from HLA Haplotyped Canadian families. Part of the data has been studied and analysed as a population; in addition there is a further random collection of Haplotypes bearing the C2*2 allele. In the population data there were 444 separate Haplotypes from unrelated parents or other founders: 4.7% of the Haplotypes carried the uncommon allele C2*2; one Haplotype carried the rare C2*3. Study of C2 2–1 heterozygotes in the population data revealed 59 Haplotypes which carried the common C2*1 allele and one which carried a deficiency allele C2*0. The remaining Haplotypes carried either C2* 1 or else an undetectable C2*0 allele. In the entire data there were 281 meioses informative for C2. The only recombinant between HLA-B and C2 showed the C2 locus to be on the DR side of the B locus. Strong allelic association between C2 *2 and Bw22 and less strong association between C2 *2 and B15 suggested the possibility of two ancestral C2 mutants. Examination of other markers on these and subsequently collected Haplotypes do not conflict with this idea since the B15 Haplotypes mostly carry C4A *4, C4B*2 whilst the Bw22 Haplotypes mostly carry C4A*4, C4B*4. The alternative idea, that there was one original mutant which crossed over from a B15 to a Bw22 Haplotype or vice versa is not excluded, however. Since approximate equilibrium has been reached between Bw22 and the HLA-A locus alleles on these C2*2 bearing Haplotypes, we conclude that this mutation is at least 5000 years old. Other Haplotypes carrying C2*2 are assumed to be ancestral recombinants; if this is true, the C2 locus map position between HLA-B and HLA-DR is confirmed. Study of C2 mutation may provide a model for understanding the genetics of some disease susceptibility genes in the HLA region.
Ryutaro Tao - One of the best experts on this subject based on the ideXlab platform.
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Molecular characterization of three non-functional S-Haplotypes in sour cherry (Prunus cerasus).
Plant molecular biology, 2006Co-Authors: Tatsuya Tsukamoto, Nathanael R Hauck, Ryutaro Tao, Ning JiangAbstract:Tetraploid sour cherry (Prunus cerasus) exhibits a genotype-dependent loss of gametophytic self-incompatibility that is caused by the accumulation of non-functional S-Haplotypes with disrupted pistil component (stylar-S) and/or pollen component (pollen-S) function. Genetic studies using diverse sour cherry germplasm identified non-functional S-Haplotypes for which an equivalent wild-type S-Haplotype was present in sweet cherry (Prunus avium), a diploid progenitor of sour cherry. In all cases, the non-functional S-Haplotype resulted from mutations affecting the stylar component S-RNase or Prunus pollen component S-Haplotype-specific F-box protein (SFB). This study determines the molecular bases of three of these S-Haplotypes that confer unilateral incompatibility, two stylar-part mutants (S 6m2 and S 13m ) and one pollen-part mutant (S 13 ′). Compared to their wild-type alleles, S 6m2 -RNase has a 1 bp deletion, S 13m -RNase has a 23 bp deletion and SFB 13 ′ has a 1 bp substitution that lead to premature stop codons. Transcripts were identified for these three alleles, S 6m2 -RNase, S 13m -RNase, and SFB 13 ′, however, these transcripts presumably result in altered proteins with a resulting loss of activity. Our characterization of natural pollen-part and stylar-part mutants in sour cherry along with other natural S-Haplotype mutants identified in Prunus supports the view that loss of pollen specificity and stylar rejection evolve independently and are caused by structural alterations affecting the S-Haplotype. The prevalence of non-functional S-Haplotypes in sour cherry but not in sweet cherry (a diploid) suggests that polyploidization and gene duplication were indirectly responsible for the dysfunction of some S-Haplotypes and the emergence of self-compatibility in sour cherry. This resembles the specific mode of evolution in yeast where accelerated evolution occurred to one member of the duplicated gene pair.
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self incompatibility s locus region of the mutated s6 Haplotype of sour cherry prunus cerasus contains a functional pollen s allele and a non functional pistil s allele
Journal of Experimental Botany, 2003Co-Authors: Hisayo Yamane, Nathanael R Hauck, Kazuo Ikeda, Amy F Iezzoni, Ryutaro TaoAbstract:This study characterizes the S 6m -Haplotype, a mutated S 6 -Haplotype with an altered HindIII cut site, of sour cherry (Prunus cerasus). Inheritance and pollination studies of S-Haplotypes from reciprocal crosses between ‘Erdi Botermo’ (EB; S 4 S 6m S a ) and ‘Rheinische Schattenmorelle’ (RS; S 6 S a S b S c ) revealed that the S 6m -Haplotype conferred unilateral incompatibility with a non-functional pistil component and a functional pollen component. Expression analyses of S 6 -RNase and SFB 6 , a candidate gene for pollen-S ,i n the S 6m -Haplotype showed that SFB 6 was transcribed in EB pollen, but S 6 -RNase was not transcribed in EB styles. These results were consistent with data from the inheritance and pollination studies. Inverse PCR for the flanking regions of S 6 -RNase in the S 6 - and S 6m -Haplotypes revealed an approximately 2600 bp insertion present at approximately 800 bp upstream of the S 6 -RNase in the S 6m -Haplotype, which is responsible for the alternation of the HindIII cut site and a possible cause of inhibition of the transcription of S 6 -RNase. SFB 6 was present downstream of S 6 -RNase in both the S 6 - and S 6m -Haplotypes and expressed in the same way, supporting the idea that SFB is a good candidate for pollen-S in Prunus.
Ning Jiang - One of the best experts on this subject based on the ideXlab platform.
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Molecular characterization of three non-functional S-Haplotypes in sour cherry (Prunus cerasus).
Plant molecular biology, 2006Co-Authors: Tatsuya Tsukamoto, Nathanael R Hauck, Ryutaro Tao, Ning JiangAbstract:Tetraploid sour cherry (Prunus cerasus) exhibits a genotype-dependent loss of gametophytic self-incompatibility that is caused by the accumulation of non-functional S-Haplotypes with disrupted pistil component (stylar-S) and/or pollen component (pollen-S) function. Genetic studies using diverse sour cherry germplasm identified non-functional S-Haplotypes for which an equivalent wild-type S-Haplotype was present in sweet cherry (Prunus avium), a diploid progenitor of sour cherry. In all cases, the non-functional S-Haplotype resulted from mutations affecting the stylar component S-RNase or Prunus pollen component S-Haplotype-specific F-box protein (SFB). This study determines the molecular bases of three of these S-Haplotypes that confer unilateral incompatibility, two stylar-part mutants (S 6m2 and S 13m ) and one pollen-part mutant (S 13 ′). Compared to their wild-type alleles, S 6m2 -RNase has a 1 bp deletion, S 13m -RNase has a 23 bp deletion and SFB 13 ′ has a 1 bp substitution that lead to premature stop codons. Transcripts were identified for these three alleles, S 6m2 -RNase, S 13m -RNase, and SFB 13 ′, however, these transcripts presumably result in altered proteins with a resulting loss of activity. Our characterization of natural pollen-part and stylar-part mutants in sour cherry along with other natural S-Haplotype mutants identified in Prunus supports the view that loss of pollen specificity and stylar rejection evolve independently and are caused by structural alterations affecting the S-Haplotype. The prevalence of non-functional S-Haplotypes in sour cherry but not in sweet cherry (a diploid) suggests that polyploidization and gene duplication were indirectly responsible for the dysfunction of some S-Haplotypes and the emergence of self-compatibility in sour cherry. This resembles the specific mode of evolution in yeast where accelerated evolution occurred to one member of the duplicated gene pair.
Nathanael R Hauck - One of the best experts on this subject based on the ideXlab platform.
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Molecular characterization of three non-functional S-Haplotypes in sour cherry (Prunus cerasus).
Plant molecular biology, 2006Co-Authors: Tatsuya Tsukamoto, Nathanael R Hauck, Ryutaro Tao, Ning JiangAbstract:Tetraploid sour cherry (Prunus cerasus) exhibits a genotype-dependent loss of gametophytic self-incompatibility that is caused by the accumulation of non-functional S-Haplotypes with disrupted pistil component (stylar-S) and/or pollen component (pollen-S) function. Genetic studies using diverse sour cherry germplasm identified non-functional S-Haplotypes for which an equivalent wild-type S-Haplotype was present in sweet cherry (Prunus avium), a diploid progenitor of sour cherry. In all cases, the non-functional S-Haplotype resulted from mutations affecting the stylar component S-RNase or Prunus pollen component S-Haplotype-specific F-box protein (SFB). This study determines the molecular bases of three of these S-Haplotypes that confer unilateral incompatibility, two stylar-part mutants (S 6m2 and S 13m ) and one pollen-part mutant (S 13 ′). Compared to their wild-type alleles, S 6m2 -RNase has a 1 bp deletion, S 13m -RNase has a 23 bp deletion and SFB 13 ′ has a 1 bp substitution that lead to premature stop codons. Transcripts were identified for these three alleles, S 6m2 -RNase, S 13m -RNase, and SFB 13 ′, however, these transcripts presumably result in altered proteins with a resulting loss of activity. Our characterization of natural pollen-part and stylar-part mutants in sour cherry along with other natural S-Haplotype mutants identified in Prunus supports the view that loss of pollen specificity and stylar rejection evolve independently and are caused by structural alterations affecting the S-Haplotype. The prevalence of non-functional S-Haplotypes in sour cherry but not in sweet cherry (a diploid) suggests that polyploidization and gene duplication were indirectly responsible for the dysfunction of some S-Haplotypes and the emergence of self-compatibility in sour cherry. This resembles the specific mode of evolution in yeast where accelerated evolution occurred to one member of the duplicated gene pair.
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self incompatibility s locus region of the mutated s6 Haplotype of sour cherry prunus cerasus contains a functional pollen s allele and a non functional pistil s allele
Journal of Experimental Botany, 2003Co-Authors: Hisayo Yamane, Nathanael R Hauck, Kazuo Ikeda, Amy F Iezzoni, Ryutaro TaoAbstract:This study characterizes the S 6m -Haplotype, a mutated S 6 -Haplotype with an altered HindIII cut site, of sour cherry (Prunus cerasus). Inheritance and pollination studies of S-Haplotypes from reciprocal crosses between ‘Erdi Botermo’ (EB; S 4 S 6m S a ) and ‘Rheinische Schattenmorelle’ (RS; S 6 S a S b S c ) revealed that the S 6m -Haplotype conferred unilateral incompatibility with a non-functional pistil component and a functional pollen component. Expression analyses of S 6 -RNase and SFB 6 , a candidate gene for pollen-S ,i n the S 6m -Haplotype showed that SFB 6 was transcribed in EB pollen, but S 6 -RNase was not transcribed in EB styles. These results were consistent with data from the inheritance and pollination studies. Inverse PCR for the flanking regions of S 6 -RNase in the S 6 - and S 6m -Haplotypes revealed an approximately 2600 bp insertion present at approximately 800 bp upstream of the S 6 -RNase in the S 6m -Haplotype, which is responsible for the alternation of the HindIII cut site and a possible cause of inhibition of the transcription of S 6 -RNase. SFB 6 was present downstream of S 6 -RNase in both the S 6 - and S 6m -Haplotypes and expressed in the same way, supporting the idea that SFB is a good candidate for pollen-S in Prunus.
W. H. Marshall - One of the best experts on this subject based on the ideXlab platform.
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study of alleles of the second complement component c2 on canadian hla Haplotypes
Tissue Antigens, 2008Co-Authors: W. H. Marshall, John M Barnard, Nadir R Farid, R Grandy, Bodil Larsen, Ronald Payne, Verna M Skanes, David N. Churchill, George Cornell Ebers, Donald W. PatyAbstract:Typing for genetic variation in the second complement component C2 was performed on sera from HLA Haplotyped Canadian families. Part of the data has been studied and analysed as a population; in addition there is a further random collection of Haplotypes bearing the C2*2 allele. In the population data there were 444 separate Haplotypes from unrelated parents or other founders: 4.7% of the Haplotypes carried the uncommon allele C2*2; one Haplotype carried the rare C2*3. Study of C2 2–1 heterozygotes in the population data revealed 59 Haplotypes which carried the common C2*1 allele and one which carried a deficiency allele C2*0. The remaining Haplotypes carried either C2* 1 or else an undetectable C2*0 allele. In the entire data there were 281 meioses informative for C2. The only recombinant between HLA-B and C2 showed the C2 locus to be on the DR side of the B locus. Strong allelic association between C2 *2 and Bw22 and less strong association between C2 *2 and B15 suggested the possibility of two ancestral C2 mutants. Examination of other markers on these and subsequently collected Haplotypes do not conflict with this idea since the B15 Haplotypes mostly carry C4A *4, C4B*2 whilst the Bw22 Haplotypes mostly carry C4A*4, C4B*4. The alternative idea, that there was one original mutant which crossed over from a B15 to a Bw22 Haplotype or vice versa is not excluded, however. Since approximate equilibrium has been reached between Bw22 and the HLA-A locus alleles on these C2*2 bearing Haplotypes, we conclude that this mutation is at least 5000 years old. Other Haplotypes carrying C2*2 are assumed to be ancestral recombinants; if this is true, the C2 locus map position between HLA-B and HLA-DR is confirmed. Study of C2 mutation may provide a model for understanding the genetics of some disease susceptibility genes in the HLA region.
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study of alleles of the second complement component c2 on canadian hla Haplotypes
Tissue Antigens, 2008Co-Authors: W. H. Marshall, John M Barnard, Nadir R Farid, R Grandy, Bodil Larsen, Ronald Payne, Verna M Skanes, David N. Churchill, George Cornell Ebers, Donald W. PatyAbstract:Typing for genetic variation in the second complement component C2 was performed on sera from HLA Haplotyped Canadian families. Part of the data has been studied and analysed as a population; in addition there is a further random collection of Haplotypes bearing the C2*2 allele. In the population data there were 444 separate Haplotypes from unrelated parents or other founders: 4.7% of the Haplotypes carried the uncommon allele C2*2; one Haplotype carried the rare C2*3. Study of C2 2–1 heterozygotes in the population data revealed 59 Haplotypes which carried the common C2*1 allele and one which carried a deficiency allele C2*0. The remaining Haplotypes carried either C2* 1 or else an undetectable C2*0 allele. In the entire data there were 281 meioses informative for C2. The only recombinant between HLA-B and C2 showed the C2 locus to be on the DR side of the B locus. Strong allelic association between C2 *2 and Bw22 and less strong association between C2 *2 and B15 suggested the possibility of two ancestral C2 mutants. Examination of other markers on these and subsequently collected Haplotypes do not conflict with this idea since the B15 Haplotypes mostly carry C4A *4, C4B*2 whilst the Bw22 Haplotypes mostly carry C4A*4, C4B*4. The alternative idea, that there was one original mutant which crossed over from a B15 to a Bw22 Haplotype or vice versa is not excluded, however. Since approximate equilibrium has been reached between Bw22 and the HLA-A locus alleles on these C2*2 bearing Haplotypes, we conclude that this mutation is at least 5000 years old. Other Haplotypes carrying C2*2 are assumed to be ancestral recombinants; if this is true, the C2 locus map position between HLA-B and HLA-DR is confirmed. Study of C2 mutation may provide a model for understanding the genetics of some disease susceptibility genes in the HLA region.
