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a previous study, we carried out a genome screen to identify QTL controlling CIA susceptibility in (DBA/1 × FVB/N) F2 progeny. For the phenotype of arthritis severity, only one QTL, Cia2, was identified, with a highly significant logarithm of the odds (LOD) score of 12 [10]. However, Cia2 contributed to only 16% of the phenotype variations, indicating that there should be some small-effect QTL whose contributions to CIA were not big enough to reach the significant threshold value of linkage. To identify these potential small-effect QTL, we reanalyzed the data using a lower threshold value of linkage (P = 0.05). We reasoned that since the main candidate gene of Cia2, complement component C5 (Hc), was proven to be essential for CIA development and because the FVB/N strain is C5 deficient [10,25], some small-effect QTL might be masked by Cia2. To exclude the masking effect of C5, we performed linkage analysis with 3 datasets, the first containing all 290 F2 progeny, the second 77 C5+/+ F2 progeny and the third 133 C5+/- F2 progeny. Eight genomic regions were linked to the phenotype of CIA severity (loci 1 to 8, Table 2), with P values varying between 0.043 and 0.003. These eight small-effect QTL were located on chromosomes 5, 6, 7, 10, 11, 16, and 17. Five loci were identified in at least two datasets. Of the eight loci, five had DBA/1 as the susceptibility allele, and three had FVB/N as the susceptibility allele."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T7026","span":{"begin":38,"end":44},"obj":"SO_EXT:0001026"},{"id":"T7027","span":{"begin":64,"end":67},"obj":"SO_EXT:0000771"},{"id":"T7028","span":{"begin":68,"end":79},"obj":"GO:0065007"},{"id":"T7029","span":{"begin":180,"end":183},"obj":"SO_EXT:0000771"},{"id":"T7030","span":{"begin":396,"end":399},"obj":"SO_EXT:0000771"},{"id":"T7031","span":{"begin":541,"end":544},"obj":"SO_EXT:0000771"},{"id":"T7032","span":{"begin":664,"end":668},"obj":"SO_EXT:0000704"},{"id":"T7033","span":{"begin":678,"end":701},"obj":"PR_EXT:000004904"},{"id":"T7034","span":{"begin":703,"end":705},"obj":"PR_EXT:000004904"},{"id":"T7035","span":{"begin":787,"end":789},"obj":"PR_EXT:000004904"},{"id":"T7036","span":{"begin":827,"end":830},"obj":"SO_EXT:0000771"},{"id":"T7037","span":{"begin":889,"end":891},"obj":"PR_EXT:000004904"},{"id":"T7038","span":{"begin":995,"end":997},"obj":"PR_EXT:000004904"},{"id":"T7039","span":{"begin":997,"end":998},"obj":"SO_EXT:normal_or_wild_type_or_present"},{"id":"T7040","span":{"begin":999,"end":1000},"obj":"SO_EXT:normal_or_wild_type_or_present"},{"id":"T7041","span":{"begin":1030,"end":1032},"obj":"PR_EXT:000004904"},{"id":"T7042","span":{"begin":1032,"end":1033},"obj":"SO_EXT:normal_or_wild_type_or_present"},{"id":"T7043","span":{"begin":1034,"end":1035},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T7044","span":{"begin":1054,"end":1061},"obj":"SO_EXT:0001026"},{"id":"T7045","span":{"begin":1211,"end":1214},"obj":"SO_EXT:0000771"},{"id":"T7046","span":{"begin":1231,"end":1242},"obj":"GO_SO_EXT:chromosome"},{"id":"T7047","span":{"begin":1380,"end":1386},"obj":"SO_EXT:0001023"},{"id":"T7048","span":{"begin":1430,"end":1436},"obj":"SO_EXT:0001023"}],"text":"In a previous study, we carried out a genome screen to identify QTL controlling CIA susceptibility in (DBA/1 × FVB/N) F2 progeny. For the phenotype of arthritis severity, only one QTL, Cia2, was identified, with a highly significant logarithm of the odds (LOD) score of 12 [10]. However, Cia2 contributed to only 16% of the phenotype variations, indicating that there should be some small-effect QTL whose contributions to CIA were not big enough to reach the significant threshold value of linkage. To identify these potential small-effect QTL, we reanalyzed the data using a lower threshold value of linkage (P = 0.05). We reasoned that since the main candidate gene of Cia2, complement component C5 (Hc), was proven to be essential for CIA development and because the FVB/N strain is C5 deficient [10,25], some small-effect QTL might be masked by Cia2. To exclude the masking effect of C5, we performed linkage analysis with 3 datasets, the first containing all 290 F2 progeny, the second 77 C5+/+ F2 progeny and the third 133 C5+/- F2 progeny. Eight genomic regions were linked to the phenotype of CIA severity (loci 1 to 8, Table 2), with P values varying between 0.043 and 0.003. These eight small-effect QTL were located on chromosomes 5, 6, 7, 10, 11, 16, and 17. Five loci were identified in at least two datasets. Of the eight loci, five had DBA/1 as the susceptibility allele, and three had FVB/N as the susceptibility allele."}

{"project":"2_test","denotations":[{"id":"17244351-15529344-4361130","span":{"begin":274,"end":276},"obj":"15529344"},{"id":"17244351-15529344-4361131","span":{"begin":801,"end":803},"obj":"15529344"},{"id":"17244351-10754334-4361132","span":{"begin":804,"end":806},"obj":"10754334"}],"text":"In a previous study, we carried out a genome screen to identify QTL controlling CIA susceptibility in (DBA/1 × FVB/N) F2 progeny. For the phenotype of arthritis severity, only one QTL, Cia2, was identified, with a highly significant logarithm of the odds (LOD) score of 12 [10]. However, Cia2 contributed to only 16% of the phenotype variations, indicating that there should be some small-effect QTL whose contributions to CIA were not big enough to reach the significant threshold value of linkage. To identify these potential small-effect QTL, we reanalyzed the data using a lower threshold value of linkage (P = 0.05). We reasoned that since the main candidate gene of Cia2, complement component C5 (Hc), was proven to be essential for CIA development and because the FVB/N strain is C5 deficient [10,25], some small-effect QTL might be masked by Cia2. To exclude the masking effect of C5, we performed linkage analysis with 3 datasets, the first containing all 290 F2 progeny, the second 77 C5+/+ F2 progeny and the third 133 C5+/- F2 progeny. Eight genomic regions were linked to the phenotype of CIA severity (loci 1 to 8, Table 2), with P values varying between 0.043 and 0.003. These eight small-effect QTL were located on chromosomes 5, 6, 7, 10, 11, 16, and 17. Five loci were identified in at least two datasets. Of the eight loci, five had DBA/1 as the susceptibility allele, and three had FVB/N as the susceptibility allele."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T6985","span":{"begin":38,"end":44},"obj":"SO:0001026"},{"id":"T6986","span":{"begin":64,"end":67},"obj":"SO:0000771"},{"id":"T6987","span":{"begin":68,"end":79},"obj":"GO:0065007"},{"id":"T6988","span":{"begin":180,"end":183},"obj":"SO:0000771"},{"id":"T6989","span":{"begin":396,"end":399},"obj":"SO:0000771"},{"id":"T6990","span":{"begin":541,"end":544},"obj":"SO:0000771"},{"id":"T6991","span":{"begin":664,"end":668},"obj":"SO:0000704"},{"id":"T6992","span":{"begin":678,"end":701},"obj":"PR:000004904"},{"id":"T6993","span":{"begin":703,"end":705},"obj":"PR:000004904"},{"id":"T6994","span":{"begin":787,"end":789},"obj":"PR:000004904"},{"id":"T6995","span":{"begin":827,"end":830},"obj":"SO:0000771"},{"id":"T6996","span":{"begin":889,"end":891},"obj":"PR:000004904"},{"id":"T6997","span":{"begin":995,"end":997},"obj":"PR:000004904"},{"id":"T6998","span":{"begin":1030,"end":1032},"obj":"PR:000004904"},{"id":"T6999","span":{"begin":1054,"end":1061},"obj":"SO:0001026"},{"id":"T7000","span":{"begin":1211,"end":1214},"obj":"SO:0000771"},{"id":"T7001","span":{"begin":1380,"end":1386},"obj":"SO:0001023"},{"id":"T7002","span":{"begin":1430,"end":1436},"obj":"SO:0001023"}],"text":"In a previous study, we carried out a genome screen to identify QTL controlling CIA susceptibility in (DBA/1 × FVB/N) F2 progeny. For the phenotype of arthritis severity, only one QTL, Cia2, was identified, with a highly significant logarithm of the odds (LOD) score of 12 [10]. However, Cia2 contributed to only 16% of the phenotype variations, indicating that there should be some small-effect QTL whose contributions to CIA were not big enough to reach the significant threshold value of linkage. To identify these potential small-effect QTL, we reanalyzed the data using a lower threshold value of linkage (P = 0.05). We reasoned that since the main candidate gene of Cia2, complement component C5 (Hc), was proven to be essential for CIA development and because the FVB/N strain is C5 deficient [10,25], some small-effect QTL might be masked by Cia2. To exclude the masking effect of C5, we performed linkage analysis with 3 datasets, the first containing all 290 F2 progeny, the second 77 C5+/+ F2 progeny and the third 133 C5+/- F2 progeny. Eight genomic regions were linked to the phenotype of CIA severity (loci 1 to 8, Table 2), with P values varying between 0.043 and 0.003. These eight small-effect QTL were located on chromosomes 5, 6, 7, 10, 11, 16, and 17. Five loci were identified in at least two datasets. Of the eight loci, five had DBA/1 as the susceptibility allele, and three had FVB/N as the susceptibility allele."}