Contribution of maternal effect QTL to genetic architecture of early growth in mice
Contribution of maternal effect QTL to genetic architecture of early growth in mice
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DOI：
10.1038/sj.hdy.6800140
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发表时间：
2002-10
期刊：
影响因子：
3.8
通讯作者：
Jason B. Wolf;Jason B. Wolf;Ty T. Vaughn;Ty T. Vaughn;L. S. Pletscher;L. S. Pletscher;J. Cheverud;J. Cheverud
中科院分区：
文献类型：
--
作者：
Jason B. Wolf;Jason B. Wolf;Ty T. Vaughn;Ty T. Vaughn;L. S. Pletscher;L. S. Pletscher;J. Cheverud;J. Cheverud
现有的方法来表征数量性状基因座（QTL）利用明确集中在基因的直接影响，其中个体之间的表型变异映射到这些个体的遗传变异的范例。然而，对于许多性状，母体基因型通过其母体效应占后代表型遗传变异的相当大的一部分。因此，对直接效应QTL的关注可能导致遗传结构的不充分或误导性表征，这是由于遗漏了母体效应所贡献的遗传方差的潜在重要来源。我们分析了直接和母体效应（ME）QTL的相对贡献，在小鼠早期生长使用三代互交的小（SM/J）和大（LG/J）近交系小鼠。利用区间作图和复合区间作图方法，在不存在母体遗传效应方差（所有个体均为遗传完全相同的F1母体的后代）的杂交F2代（n= 510）中检测到了早期生长（1 ~ 2周龄体重变化）的直接效应QTL。将F3代杂种后代的表型作为其母代的特征进行了ME QTL的检测。检测到5个在染色体水平上显著（α= 0.05）的DE QTL，其中2个在基因组水平上显著。检测到4个在染色体水平上显著的QTL，其中3个在基因组水平上显著。仅含DE QTL的模型可解释11.8%的表型方差，而仅含ME QTL的模型可解释31.5%的窝间生长方差。没有证据表明DE和ME基因座的多效性，因为在这两个分析中检测到的基因座之间没有重叠。所有对基因座之间的上位性进行了分析DE和ME。十对基因座对ME表现出显着的上位性（多重比较校正后的α= 0.05），而四对基因座对DE在早期生长上表现出显着的上位性。
Existing approaches to characterizing quantitative trait loci (QTL) utilize a paradigm explicitly focused on the direct effects of genes, where phenotypic variation among individuals is mapped onto genetic variation of those individuals. For many characters, however, the genotype of the mother via its maternal effect accounts for a considerable portion of the genetically based variation in progeny phenotypes. Thus the focus on direct effect QTL may result in an insufficient or misleading characterization of genetic architecture due to the omission of the potentially important source of genetic variance contributed by maternal effects. We analyze the relative contribution of direct and maternal effect (ME) QTL to early growth in mice using a three-generation intercross of the Small (SM/J) and Large (LG/J) inbred mouse lineages. Using interval mapping and composite interval mapping, direct effect (DE) QTL for early growth (change in body mass during the interval from week 1 to 2) were detected in the F 2 generation of the intercross (n= 510), where no maternal genetic effect variance is present (all individuals are progeny of genetically identical F 1 mothers). ME QTL were detected by treating the phenotypes of cross-fostered F 3 pups as a characteristic of their nurse-dam (n= 168 dams with cross-fostered progeny). Five DE QTL, significant at a chromosome wide level (α= 0.05), were detected, with two significant at a genome wide level. FourME QTL significant at the chromosome wide level were detected, with three significant at the genome wide level. A model containing only DE QTL accounted for 11.8% of phenotypic variance, while a model containing only ME QTL accounted for 31.5% of the among litter variance in growth. There was no evidence for pleiotropy of DE and ME loci since there was no overlap between loci detected in these two analyses. Epistasis between all pairs of loci was analyzed for both DEs and MEs. Ten pairs of loci showed significant epistasis for MEs (α= 0.05 corrected for multiple comparisons) while four pairs showed significant epistasis for DEs on early growth.