Bioinformatics Centre, Bose Institute, P 1/12, C.I.T. Scheme VII M, Kolkata 700 054, India.
Genomics. 2011 Apr;97(4):200-4. doi: 10.1016/j.ygeno.2011.01.004. Epub 2011 Jan 31.
Functional redundancy by gene duplication appears to be a common phenomenon in biological system and hence understanding its underlying mechanism deserves much attention. Here, we investigated the differences between functional compensation of monogenic and polygenic disease genes which are unexplored till date. We found that the competence of functional buffering varies in the order of non-disease genes>monogenic disease genes>polygenic disease genes. This fact has been explained by the sequence identity, expression profile similarity, shared interaction partners and cellular locations between duplicated pairs. Moreover, we observed an inverse relationship between backup capacity and the non-synonymous substitution rate of disease and non-disease genes while the opposite trend is found for their corresponding paralogs. Logistic regression analysis among sequence identity, sharing of expression profile, interaction partners and cellular locations with backup capacity between duplicated pairs demonstrated that the sharing of expression profile is the most dominant regulator of backup capacity.
功能冗余通过基因复制似乎是一种常见的现象在生物系统中，因此理解其潜在的机制值得关注。在这里，我们研究了单基因和多基因疾病基因的功能补偿之间的差异，这在迄今为止的研究中尚未得到探索。我们发现，功能缓冲的能力按非疾病基因>单基因疾病基因>多基因疾病基因的顺序变化。这一事实可以通过重复对之间的序列同一性、表达谱相似性、共享相互作用伙伴和细胞位置来解释。此外，我们观察到备份能力与疾病和非疾病基因的非同义替换率之间存在反比关系，而其相应的旁系同源物则呈现相反的趋势。重复对之间的序列同一性、表达谱共享、相互作用伙伴和细胞位置与备份能力之间的逻辑回归分析表明，表达谱的共享是备份能力的最主要调节因子。
