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It is now widely recognized that robustness is an inherent property of biological systems  [1] , [2] , [3] . The contribution of close sequence homologs to genetic robustness against null mutations has been previously demonstrated in simple organisms  [4] , [5] . In this paper we investigate in detail the contribution of gene duplicates to back-up against deleterious human mutations. Our analysis demonstrates that the functional compensation by close homologs may play an important role in human genetic disease. Genes with a 90% sequence identity homolog are about 3 times less likely to harbor known disease mutations compared to genes with remote homologs. Moreover, close duplicates affect the phenotypic consequences of deleterious mutations by making a decrease in life expectancy significantly less likely. We also demonstrate that similarity of expression profiles across tissues significantly increases the likelihood of functional compensation by homologs.

Role of Duplicate Genes in Robustness against Deleterious Human Mutations