2024-03-28T19:58:17Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/489002019-11-06T13:51:02Zcom_10261_103com_10261_1col_10261_356
00925njm 22002777a 4500
dc
Sanjuán, Rafael
author
Nebot, Miguel R.
author
2008-07-16
The study of genetic interactions (epistasis) is central to the understanding of genome organization and evolution. A
general correlation between epistasis and genomic complexity has been recently shown, such that in simpler genomes
epistasis is antagonistic on average (mutational effects tend to cancel each other out), whereas a transition towards
synergistic epistasis occurs in more complex genomes (mutational effects strengthen each other). Here, we use a simple
network model to identify basic features explaining this correlation. We show that, in small networks with multifunctional
nodes, lack of redundancy, and absence of alternative pathways, epistasis is antagonistic on average. In contrast, lack of
multi-functionality, high connectivity, and redundancy favor synergistic epistasis. Moreover, we confirm the previous finding
that epistasis is a covariate of mutational robustness: in less robust networks it tends to be antagonistic whereas in more
robust networks it tends to be synergistic. We argue that network features associated with antagonistic epistasis are
typically found in simple genomes, such as those of viruses and bacteria, whereas the features associated with synergistic
epistasis are more extensively exploited by higher eukaryotes.
PLoS ONE 3/7: e2663 (2008)
http://hdl.handle.net/10261/48900
10.1371/journal.pone.0002663
1932-6203
18648534
A Network Model for the Correlation between Epistasis and Genomic Complexity