Defense against infection incurs costs as well as benefits that are expected to shape the evolution of optimal defense
strategies. In particular, many theoretical studies have investigated contexts favoring constitutive versus inducible
defenses. However, even when one immune strategy is theoretically optimal, it may be evolutionarily unachievable.
This is because evolution proceeds via mutational changes to the protein interaction networks underlying immune
responses, not by changes to an immune strategy directly. Here, we use a theoretical simulation model to examine how
underlying network architectures constrain the evolution of immune strategies, and how these network architectures
account for desirable immune properties such as inducibility and robustness. We focus on immune signaling because
signaling molecules are common targets of parasitic interference but are rarely studied in this context. We find that in the
presence of a coevolving parasite that disrupts immune signaling, hosts evolve constitutive defenses even when inducible
defenses are theoretically optimal. This occurs for two reasons. First, there are relatively few network architectures that
produce immunity that is both inducible and also robust against targeted disruption. Second, evolution toward these few
robust inducible network architectures often requires intermediate steps that are vulnerable to targeted disruption. The
few networks that are both robust and inducible consist of many parallel pathways of immune signaling with few
connections among them. In the context of relevant empirical literature, we discuss whether this is indeed the most
evolutionarily accessible robust inducible network architecture in nature, and when it can evolve.
%0 Journal Article
%1 schrom2018immune
%A Schrom, Edward C
%A Prada, Joaquín M
%A Graham, Andrea L
%D 2018
%J Molecular Biology and Evolution
%K network_evolution robustness simulation
%N 3
%P 676-687
%R 10.1093/molbev/msx321
%T Immune Signaling Networks: Sources of Robustness and Constrained Evolvability during Coevolution
%U http://dx.doi.org/10.1093/molbev/msx321
%V 35
%X Defense against infection incurs costs as well as benefits that are expected to shape the evolution of optimal defense
strategies. In particular, many theoretical studies have investigated contexts favoring constitutive versus inducible
defenses. However, even when one immune strategy is theoretically optimal, it may be evolutionarily unachievable.
This is because evolution proceeds via mutational changes to the protein interaction networks underlying immune
responses, not by changes to an immune strategy directly. Here, we use a theoretical simulation model to examine how
underlying network architectures constrain the evolution of immune strategies, and how these network architectures
account for desirable immune properties such as inducibility and robustness. We focus on immune signaling because
signaling molecules are common targets of parasitic interference but are rarely studied in this context. We find that in the
presence of a coevolving parasite that disrupts immune signaling, hosts evolve constitutive defenses even when inducible
defenses are theoretically optimal. This occurs for two reasons. First, there are relatively few network architectures that
produce immunity that is both inducible and also robust against targeted disruption. Second, evolution toward these few
robust inducible network architectures often requires intermediate steps that are vulnerable to targeted disruption. The
few networks that are both robust and inducible consist of many parallel pathways of immune signaling with few
connections among them. In the context of relevant empirical literature, we discuss whether this is indeed the most
evolutionarily accessible robust inducible network architecture in nature, and when it can evolve.
@article{schrom2018immune,
abstract = {Defense against infection incurs costs as well as benefits that are expected to shape the evolution of optimal defense
strategies. In particular, many theoretical studies have investigated contexts favoring constitutive versus inducible
defenses. However, even when one immune strategy is theoretically optimal, it may be evolutionarily unachievable.
This is because evolution proceeds via mutational changes to the protein interaction networks underlying immune
responses, not by changes to an immune strategy directly. Here, we use a theoretical simulation model to examine how
underlying network architectures constrain the evolution of immune strategies, and how these network architectures
account for desirable immune properties such as inducibility and robustness. We focus on immune signaling because
signaling molecules are common targets of parasitic interference but are rarely studied in this context. We find that in the
presence of a coevolving parasite that disrupts immune signaling, hosts evolve constitutive defenses even when inducible
defenses are theoretically optimal. This occurs for two reasons. First, there are relatively few network architectures that
produce immunity that is both inducible and also robust against targeted disruption. Second, evolution toward these few
robust inducible network architectures often requires intermediate steps that are vulnerable to targeted disruption. The
few networks that are both robust and inducible consist of many parallel pathways of immune signaling with few
connections among them. In the context of relevant empirical literature, we discuss whether this is indeed the most
evolutionarily accessible robust inducible network architecture in nature, and when it can evolve.},
added-at = {2018-11-02T20:59:59.000+0100},
author = {Schrom, Edward C and Prada, Joaquín M and Graham, Andrea L},
biburl = {https://www.bibsonomy.org/bibtex/26c820ad27fb37b2ac8a0990d340f6900/peter.ralph},
doi = {10.1093/molbev/msx321},
eprint = {/oup/backfile/content_public/journal/mbe/35/3/10.1093_molbev_msx321/2/msx321.pdf},
interhash = {50230f225411076072a25c4559a75a72},
intrahash = {6c820ad27fb37b2ac8a0990d340f6900},
journal = {Molecular Biology and Evolution},
keywords = {network_evolution robustness simulation},
number = 3,
pages = {676-687},
timestamp = {2018-11-02T21:01:23.000+0100},
title = {Immune Signaling Networks: Sources of Robustness and Constrained Evolvability during Coevolution},
url = {http://dx.doi.org/10.1093/molbev/msx321},
volume = 35,
year = 2018
}