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非肥胖糖尿病小鼠品系及其非糖尿病姐妹品系主要组织相容性复合体基因的限制性片段长度多态性分析。

Restriction fragment length polymorphism analysis of major histocompatibility complex genes in the non-obese diabetic mouse strain and its non-diabetic sister strains.

作者信息

Fujishima Y, Koide Y, Kaidoh T, Nishimura M, Yoshida T O

机构信息

Department of Microbiology and Immunology, Hamamatsu University School of Medicine, Japan.

出版信息

Diabetologia. 1989 Feb;32(2):118-25. doi: 10.1007/BF00505184.

Abstract

It has been suggested that one of the recessive genes controlling diabetes in non-obese diabetic mice is linked to the major histocompatibility complex. We, therefore, performed restriction fragment length polymorphism studies of major histocompatibility complex genes (class I, II, and III) in non-obese diabetic mice in comparison with those of their non-diabetic sister strains, non-obese non-diabetic, cataract, and ILI mice which were derived from the same Jcl-ICR mice as the non-obese diabetic mouse was. When class II and III probes and a minimum of four restriction enzymes were used, class II and III genes of non-obese diabetic mice were indistinguishable from those of cataract and ILI mice but totally different from those of non-obese non-diabetic mice. The studies also indicated that A beta, E beta, and C4-Slp genes of non-obese diabetic, cataract, and ILI mice, and A alpha, A beta, E beta and C4-Slp genes of non-obese non-diabetic mice are different from those of BALB/c and C57BL/6 mice, respectively. While non-obese non-diabetic mice expressed the E alpha gene, non-obese diabetic, cataract, and ILI mice appeared to carry a deletion in the 5' end of the E alpha gene resulting in failure to transcribe the E alpha gene. When class I probe was used, cataract mice showed very different band patterns from those of the other ICR-derived mice. It is suggested that non-obese diabetic, non-obese non-diabetic, and ILI mice contain only a single class I D region gene.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

有人提出,控制非肥胖型糖尿病小鼠糖尿病的隐性基因之一与主要组织相容性复合体相关。因此,我们对非肥胖型糖尿病小鼠的主要组织相容性复合体基因(I类、II类和III类)进行了限制性片段长度多态性研究,并与它们的非糖尿病姐妹品系非肥胖非糖尿病小鼠、白内障小鼠和ILI小鼠进行了比较,这些品系均源自与非肥胖型糖尿病小鼠相同的Jcl-ICR小鼠。当使用II类和III类探针以及至少四种限制性内切酶时,非肥胖型糖尿病小鼠的II类和III类基因与白内障小鼠和ILI小鼠的基因无法区分,但与非肥胖非糖尿病小鼠的基因完全不同。研究还表明,非肥胖型糖尿病小鼠、白内障小鼠和ILI小鼠的Aβ、Eβ和C4-Slp基因,以及非肥胖非糖尿病小鼠的Aα、Aβ、Eβ和C4-Slp基因分别与BALB/c和C57BL/6小鼠的基因不同。非肥胖非糖尿病小鼠表达Eα基因,而非肥胖型糖尿病小鼠、白内障小鼠和ILI小鼠似乎在Eα基因的5'端存在缺失,导致无法转录Eα基因。当使用I类探针时,白内障小鼠显示出与其他源自ICR的小鼠非常不同的条带模式。有人提出,非肥胖型糖尿病小鼠、非肥胖非糖尿病小鼠和ILI小鼠仅含有一个I类D区域基因。(摘要截取自250字)

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