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Nucleic Acids Research Advance Access published online on September 18, 2007
Nucleic Acids Research, doi:10.1093/nar/gkm723
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© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Computational Biology

Organismal complexity, cell differentiation and gene expression: human over mouse

Alexander E. Vinogradov* and Olga V. Anatskaya

Institute of Cytology, Russian Academy of Sciences, Tikhoretsky Avenue 4, St. Petersburg 194064, Russia

*To whom correspondence should be addressed. Tel: +7-812-2971452; Fax: +7-812-2970341; Email: aevin{at}mail.cytspb.rssi.ru

Received July 2, 2007. Revised August 12, 2007. Accepted September 1, 2007.

We present a molecular and cellular phenomenon underlying the intriguing increase in phenotypic organizational complexity. For the same set of human–mouse orthologous genes (11 534 gene pairs) and homologous tissues (32 tissue pairs), human shows a greater fraction of tissue-specific genes and a greater ratio of the total expression of tissue-specific genes to housekeeping genes in each studied tissue, which suggests a generally higher level of evolutionary cell differentiation (specialization). This phenomenon is spectacularly more pronounced in those human tissues that are more directly involved in the increase of complexity, longevity and body size (i.e. it is reflected on the organismal level as well). Genes with a change in expression breadth show a greater human–mouse divergence of promoter regions and encoded proteins (i.e. the functional genomics data are supported by the structural analysis). Human also shows the higher expression of translation machinery. The upstream untranslated regions (5'UTRs) of human mRNAs are longer than mouse 5'UTRs (even after correction for the difference in genome sizes) and contain more uAUG codons, which suggest a more complex regulation at the translational level in human cells (and agrees well with the augmented cell specialization).


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