Fukushima Sanae, Niimi Kimie, Takahashi Eiki
Research Resources Center, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
J Vet Med Sci. 2015 Feb;77(2):161-6. doi: 10.1292/jvms.14-0408. Epub 2014 Oct 20.
The classic piebald mutation in the endothelin receptor type B (Ednrb) gene was found on rolling Nagoya genetic background (PROD-s/s) mice with white coat spotting. To examine whether genetic background influenced the phenotype in the piebald mutant mice, we generated a congenic strain (B6.PROD-s/s), produced by repeated backcrosses to the C57BL/6J (B6) strain. Although B6.PROD-s/s mice showed white coat spotting, 7% of B6.PROD-s/s mice died between 2 and 5 weeks after birth due to megacolon. The PROD-s/s, s/s and Japanese fancy mouse 1 (JF1) strains, which also have piebald mutations on different genetic backgrounds with B6, showed only pigmentation defects without megacolon. In expression analyses, rectums of B6.PROD-s/s with megacolon mice showed ~5% of the level of Ednrb gene expression versus B6 mice. In histological analyses, aganglionosis was detected in the rectum of megacolon animals. The aganglionic rectum was thought to lead to severe constipation and intestinal blockage, resulting in megacolon. We also observed an abnormal intestinal flora, including a marked increase in Bacteroidaceae and Erysipelotrichaceae and a marked decrease in Lactobacillus and Clostridiales, likely inducing endotoxin production and a failure of the mucosal barrier system, leading ultimately to death. These results indicate that the genetic background plays a key role in the development of enteric ganglion neurons, controlled by the Ednrb gene, and that B6 has modifier gene (s) regarding aganglionosis.
在内皮素B型受体(Ednrb)基因中的经典花斑突变是在具有白色被毛斑点的滚动名古屋遗传背景(PROD-s/s)小鼠中发现的。为了研究遗传背景是否影响花斑突变小鼠的表型,我们培育了一个近交系(B6.PROD-s/s),通过与C57BL/6J(B6)品系反复回交产生。尽管B6.PROD-s/s小鼠表现出白色被毛斑点,但7%的B6.PROD-s/s小鼠在出生后2至5周因巨结肠死亡。PROD-s/s、s/s和日本观赏小鼠1(JF1)品系,它们在与B6不同的遗传背景上也有花斑突变,仅表现出色素沉着缺陷而无巨结肠。在表达分析中,患有巨结肠的B6.PROD-s/s小鼠的直肠中Ednrb基因表达水平相对于B6小鼠约为5%。在组织学分析中,在巨结肠动物的直肠中检测到无神经节症。无神经节的直肠被认为会导致严重便秘和肠道阻塞,从而导致巨结肠。我们还观察到肠道菌群异常,包括拟杆菌科和丹毒丝菌科显著增加,而乳酸杆菌和梭菌目显著减少,这可能诱导内毒素产生和黏膜屏障系统功能障碍,最终导致死亡。这些结果表明,遗传背景在由Ednrb基因控制的肠神经节神经元发育中起关键作用,并且B6具有关于无神经节症的修饰基因。