Evolving protein interaction networks through gene duplication.

By Romualdo Pastor-Satorras, Eric Smith, R. V. Solé. Journal of Theoretical Biology, 2003

433 citations recorded by the source corpus.

The topology of the proteome map revealed by recent large-scale hybridization methods has shown that the distribution of protein-protein interactions is highly heterogeneous, with many proteins having few edges while a few of them are heavily connected. This particular topology is shared by other cellular networks, such as metabolic pathways, and it has been suggested to be responsible for the high mutational homeostasis displayed by the genome of some organisms. In this paper we explore a recent model of proteome evolution that has been shown to reproduce many of the features displayed by its real counterparts. The model is based on gene duplication plus re-wiring of the newly created genes. The statistical features displayed by the proteome of well-known organisms are reproduced and suggest that the overall topology of the protein maps naturally emerges from the two leading mechanisms considered by the model.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e1f72ebeffbd82530ec12771b43688cc0cc662db

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

The Matthew effect in empirical data (2014, background): “The argument in favour of randomness gains traction when cognition and reasoning obviously no longer apply — consider the emergence of hubs in protein-interaction networks through gene duplication [160] (see also [61] for a thorough discussion).”
Functional Divergence of Duplicated Genes Formed by Polyploidy during Arabidopsis Evolution (2004, background): “Biochemical pathways or protein complexes could then be expressed at different times or in different places with two different but specialized sets of genes (Caffrey et al., 1999; Pastor-Satorras et al., 2003; Ihmels et al., 2004).”
Analyzing and modeling real-world phenomena with complex networks: a survey of applications (2007, methodology): “proposed a similar model with the same concepts [370], which is given in detail in [371].”
Scale-free networks in cell biology (2005, background): “Several growing network models based on random gene duplication and subsequent functional divergence have displayed good agreement with the topology of protein interaction networks (Kim et al., 2002; Pastor-Satorras et al., 2003; Vazquez A, 2003).”
Turning a hobby into a job: How duplicated genes find new functions (2008, background): “Notably, however, these models only reproduce the observed degree distributions when duplications are followed by pruning of duplicated interaction”
Selection, Tinkering, and Emergence in Complex Networks - Crossing the Land of Tinkering (2002, methodology): “…the genome/proteome evolution: the growth of these nets takes place by gene duplication (Ohono, 1970) and simple models based on gene duplication plus re-wiring successfully reproduce the observed properties of proteome maps (Sol¶e et al. , 2001; Vazquez et al, 2001; Pastor-Satorras et al. , 2002).”
Comparative Genomics in Eukaryotes (2005, methodology): “When seeding this model with a scale-free network, most of the structure persists for a few iterations; however, simulating this model for a higher number of iterations results in an exponential degree distribution of N versus k (Pastor-Satorras et al., 2003).”