Bost B, de Vienne D, Hospital F, Moreau L, Dillmann C
Station de Génétique Végétale, INRA/UPS/INA P-G, F-91190 Gif sur Yvette, France.
Genetics. 2001 Apr;157(4):1773-87. doi: 10.1093/genetics/157.4.1773.
The L-shaped distribution of estimated QTL effects (R(2)) has long been reported. We recently showed that a metabolic mechanism could account for this phenomenon. But other nonexclusive genetic or nongenetic causes may contribute to generate such a distribution. Using analysis and simulations of an additive genetic model, we show that linkage disequilibrium between QTL, low heritability, and small population size may also be involved, regardless of the gene effect distribution. In addition, a comparison of the additive and metabolic genetic models revealed that estimates of the QTL effects for traits proportional to metabolic flux are far less robust than for additive traits. However, in both models the highest R(2)'s repeatedly correspond to the same set of QTL.
长期以来,人们一直报道估计的数量性状基因座效应(R(2))呈L形分布。我们最近表明,一种代谢机制可以解释这一现象。但其他非排他性的遗传或非遗传原因可能也有助于产生这种分布。通过对加性遗传模型的分析和模拟,我们表明,无论基因效应分布如何,数量性状基因座之间的连锁不平衡、低遗传力和小群体规模也可能起作用。此外,对加性和代谢遗传模型的比较表明,与代谢通量成比例的性状的数量性状基因座效应估计值远不如加性性状的估计值稳健。然而,在这两种模型中,最高的R(2)值反复对应于同一组数量性状基因座。