Ikeda A, Zheng Q Y, Rosenstiel P, Maddatu T, Zuberi A R, Roopenian D C, North M A, Naggert J K, Johnson K R, Nishina P M
The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.
Hum Mol Genet. 1999 Sep;8(9):1761-7. doi: 10.1093/hmg/8.9.1761.
Quantitative trait locus (QTL) analysis of genetic crosses has proven to be a useful tool for identifying loci associated with specific phenotypes and for dissecting genetic components of complex traits. Inclusion of a mutation that interacts epistatically with QTLs in genetic crosses is a unique and potentially powerful method of revealing the function of novel genes and pathways. Although we know that a mutation within the novel tub gene leads to obesity and cochlear and retinal degeneration, the biological function of the gene and the mechanism by which it induces its phenotypes are not known. In the current study, a QTL analysis for auditory brainstem response (ABR) thresholds, which indicates hearing ability, was performed in tubby mice from F(2)intercrosses between C57BL/6J- tub / tub and AKR/J-+/+ F(1)hybrids (AKR intercross) and between C57BL/6J- tub / tub and CAST/Ei.B6- tub / tub F(1)hybrids (CAST intercross). A major QTL, designated asmodifieroftubbyhearing1 ( moth1 ), was identified on chromosome 2 with a LOD score of 33.4 ( P < 10(-33)) in the AKR intercross (181 mice) and of 6.0 ( P < 10(-6)) in the CAST intercross (46 mice). This QTL is responsible for 57 and 43% of ABR threshold variance, respectively, in each strain combination. In addition, a C57BL/6J congenic line carrying a 129/Ola segment encompassing the described QTL region when made homozygous for tubby also exhibits normal hearing ability. We hypothesize that C57BL/6J carries a recessive mutation of the moth1 gene which interacts with the tub mutation to cause hearing loss in tub / tub mice. A moth1 allele from either AKR/J, CAST/Ei or 129/Ola is sufficient to protect C57BL/6J- tub / tub mice from hearing loss.
对遗传杂交进行数量性状基因座(QTL)分析已被证明是一种有用的工具,可用于识别与特定表型相关的基因座,并剖析复杂性状的遗传成分。在遗传杂交中纳入一个与QTL发生上位性相互作用的突变,是揭示新基因和通路功能的一种独特且可能强大的方法。尽管我们知道新的tub基因内的一个突变会导致肥胖以及耳蜗和视网膜退化,但该基因的生物学功能及其诱导表型的机制尚不清楚。在当前研究中,对来自C57BL/6J-tub/tub和AKR/J-+/+ F1杂种(AKR回交)以及C57BL/6J-tub/tub和CAST/Ei.B6-tub/tub F1杂种(CAST回交)的F2代互交的肥胖小鼠进行了听觉脑干反应(ABR)阈值的QTL分析,ABR阈值可指示听力能力。在AKR回交(181只小鼠)中,在2号染色体上鉴定出一个主要QTL,命名为肥胖听力修饰因子1(moth1),LOD得分为33.4(P < 10-33);在CAST回交(46只小鼠)中,LOD得分为6.0(P < 10-6)。在每种品系组合中,该QTL分别导致ABR阈值变异的57%和43%。此外,当携带包含所述QTL区域的129/Ola片段的C57BL/6J近交系对肥胖基因纯合时,也表现出正常的听力能力。我们假设C57BL/