Bioinformatical assay of human gene morbidity

• Published in: Nucleic acids research Vol. 32; no. 5; pp. 1731 - 1737
• Main Authors: Kondrashov, Fyodor A., Ogurtsov, Aleksey Y., Kondrashov, Alexey S.
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 2004; Oxford Publishing Limited (England)
• Subjects: Computational Biology; Genes; Genetic Predisposition to Disease; Humans; Morbidity; Neural Networks (Computer)
• ISSN: 0305-1048; 1362-4962; 1362-4962
• DOI: 10.1093/nar/gkh330

Only a fraction of eukaryotic genes affect the phenotype drastically. We compared 18 parameters in 1273 human morbid genes, known to cause diseases, and in the remaining 16 580 unambiguous human genes. Morbid genes evolve more slowly, have wider phylogenetic distributions, are more similar to essential genes of Drosophila melanogaster, code for longer proteins containing more alanine and glycine and less histidine, lysine and methionine, possess larger numbers of longer introns with more accurate splicing signals and have higher and broader expressions. These differences make it possible to classify as non‐morbid 34% of human genes with unknown morbidity, when only 5% of known morbid genes are incorrectly classified as non‐morbid. This classification can help to identify disease‐causing genes among multiple candidates.