日前，Nature雜誌在線發表了西班牙研究者在預測基因突變後果的方法方面的研究成果。
基因決定論的局限性在臨床上（如雙胞胎的相同基因損傷卻會產生不相同的後果）和在實驗室中（如突變即便是在同質化環境中也會在同基因的動物中產生不同效應）都早已明顯表現出來了。
從認為人們也許有可能預測不同表現型這樣一個假設出發，Ben Lehner及其同事建立了一個直接預測發育中的動物的突變後果的方法。他們利用一種非侵入性的、基於螢光的方法來監測線蟲胚胎發育過程中的基因表達，並回顧性地將各個胚胎中的分子噪音與各自成年個體中的表現型進行了比較。於是，他們便識別出了兩個調控性補償機制：一個出現在密切相關的基因中；另一個涉及伴護分子等普遍性調控因子。根據這些補償的強度，可以預測每個動物個體的成年表現型。（生物谷Bioon.com）
Predicting mutation outcome from early stochastic variation in genetic interaction partners
Alejandro Burga, M. Olivia Casanueva & Ben Lehner
Many mutations, including those that cause disease, only have a detrimental effect in a subset of individuals. The reasons for this are usually unknown, but may include additional genetic variation and environmental risk factors1. However, phenotypic discordance remains even in the absence of genetic variation, for example between monozygotic twins2, and incomplete penetrance of mutations is frequent in isogenic model organisms in homogeneous environments3, 4. Here we propose a model for incomplete penetrance based on genetic interaction networks5, 6. Using Caenorhabditis elegans as a model system, we identify two compensation mechanisms that vary among individuals and influence mutation outcome. First, feedback induction of an ancestral gene duplicate differs across individuals, with high expression masking the effects of a mutation. This supports the hypothesis that redundancy is maintained in genomes to buffer stochastic developmental failure7. Second, during normal embryonic development we find that there is substantial variation in the induction of molecular chaperones such as Hsp90 (DAF-21). Chaperones act as promiscuous buffers of genetic variation8, 9, and embryos with stronger induction of Hsp90 are less likely to be affected by an inherited mutation. Simultaneously quantifying the variation in these two independent responses allows the phenotypic outcome of a mutation to be more accurately predicted in individuals. Our model and methodology provide a framework for dissecting the causes of incomplete penetrance. Further, the results establish that inter-individual variation in both specific and more general buffering systems combine to determine the outcome inherited mutations in each individual.