TY - JOUR
T1 - Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice
T2 - Additive and hierarchical properties of polygenic inheritance
AU - Nishihara, Miyuki
AU - Terada, Miho
AU - Kamogawa, Junji
AU - Ohashi, Yuichi
AU - Mori, Shiro
AU - Nakatsuru, Shuichi
AU - Nakamura, Yusuke
AU - Nose, Masato
PY - 1999/12
Y1 - 1999/12
N2 - Objective. To clarify the mode of inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr x C3H/lpr)F1 intercross, and MRL/lpr x (MRL/lpr x C3H/lpr)F1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of polygenic inheritance, possibly involving allelic polymorphism.
AB - Objective. To clarify the mode of inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr x C3H/lpr)F1 intercross, and MRL/lpr x (MRL/lpr x C3H/lpr)F1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of polygenic inheritance, possibly involving allelic polymorphism.
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U2 - 10.1002/1529-0131(199912)42:12<2616::AID-ANR16>3.0.CO;2-O
DO - 10.1002/1529-0131(199912)42:12<2616::AID-ANR16>3.0.CO;2-O
M3 - Article
C2 - 10616009
AN - SCOPUS:0033505045
VL - 42
SP - 2616
EP - 2623
JO - Arthritis and Rheumatism
JF - Arthritis and Rheumatism
SN - 0004-3591
IS - 12
ER -