Increased structural disorder of proteins encoded on human sex chromosomes.

TitleIncreased structural disorder of proteins encoded on human sex chromosomes.
Publication TypeJournal Article
Year of Publication2012
AuthorsHegyi, H., and P. Tompa
JournalMol Biosyst
Volume8
Issue1
Pagination229-36
Date Published2012 Jan
Type of Articleidp
ISSN1742-2051
KeywordsAnimals, Chromosomes, Human, Cluster Analysis, Databases, Protein, Humans, Mice, Organ Specificity, Protein Binding, Protein Conformation, Protein Folding, Protein Interaction Maps, Proteins, Proteome, Sex Chromosomes, Synteny
Abstract

Intrinsic protein disorder has been studied with respect to the chromosomal location of each protein in the human proteome and also in other fully sequenced organisms. We found that in all studied mammalian species the sex chromosome-coded proteins were significantly more disordered than the autosome-coded ones, the strongest discrepancy being observed in humans. In explaining this phenomenon we analyzed local chromosomal features and found that (1) the autosomes have a stronger correlation between the GC content of the transcripts and the structural disorder of the coded proteins than the sex chromosomes; (2) the neighbors' protein disorder correlates the strongest on the sex chromosomes; (3) the GO functions on chromosome X are somewhat biased towards functions with higher disorder but do not account for the entire phenomenon; (4) the protein-protein interactions show a non-random chromosomal distribution, the Y chromosome-coded proteins having the lowest overall frequency for interactions but the largest bias towards intra-chromosomal interactions. Tissue-specific distributions showed the most protein disorder for sex-chromosome coded proteins expressed in the testis and the ovary. We raise the possibility that the high disorder of X- and Y-encoded proteins facilitates the fast evolution of testis- and cancer-specific antigenic protein clusters on these chromosomes, in relation to their immunogenic properties and likely contribution to speciation.

DOI10.1039/c1mb05285c
Alternate JournalMol Biosyst
PubMed ID22105808