Plasticity and the evolution of gene regulatory networks and RNA secondary structures.
Phenotypic plasticity is a genotype's ability to produce distinct phenotypic variants in response to non-genetic perturbations such as alterations in the environment. Pertinent examples concern sex determination by temperature in reptiles or the induction by predators of defensive structures in the crustacean Daphnia. Plasticity may play an important role in evolution through a process called genetic assimilation (GA). If an environmental factor induces the development of a beneficial trait in some of the organisms in a population, selection will favour those alleles that increase an organism's proclivity to produce the beneficial trait. As the frequency of those alleles grows, and as new mutations and gene combinations appear, the development of the beneficial trait occurs more easily. Eventually, the beneficial trait becomes genetically fixed: it does not require induction by an environmental factor.
Many recent and diverse examples in natural populations suggest that GA may often occur. However, it merely may be that scientists are very efficient for finding the exceptional cases where GA has occurred. We argue that a frequent usage of GA by evolution requires that those genotypes that produce a new phenotype after non-genetic perturbation usually had easy access, through random genetic change, to genotypes where the same phenotype is genetically determined. Our research already supports that mutation and recombination provide such an easy access to GA in gene regulatory networks. Other research suggests the same for RNA secondary structures. Thus, plasticity may be able to steer evolutionary trajectories. Is this the case? Would evolution be directed more often towards genetic determination of a beneficial phenotype initially produced through plasticity than to other equally beneficial phenotypes? What conditions, phenotypes, properties and population parameters enhance or diminish the ability of plasticity to set the course of evolution?
Transcription factor duplication and innovation in gene regulatory networks.
Most new genes arise through gene duplication. Gene duplicates often accumulate mutations that eventually cripple them. Notwithstanding, some duplicates persist, bearing the potential to evolve new functions. Indeed, there is substantial evidence that gene duplication may be a most important factor in evolution.
Transcription factor duplication (TFD) is specially relevant as it results in the modification of gene regulatory networks. Many studies address the fate of duplicates but there is little work on how the effects of TFD permeate into whole gene regulatory networks. Considering such a network context opens new questions concerning the relationship between duplication, developmental bias, evolvability and evolutionary trajectories.
TFD may have significant effects in the evolution of mutational robustness, a genotype's ability to produce the same phenotype in the face of mutations. One might expect that, since gene duplication produces `gene back-ups', it may also increase an organism's robustness to mutations. However, this is not always the case because there are also reports that gene duplication can decrease such robustness. Do gene networks that are robust to mutations and non-genetic perturbations also tend to be robust to TFD? Does TFD tends to increase a network's tolerance to mutations? In case there is such an effect, is it merely a consequence of increasing the number of genes or is it specific to TFD?
TFD may also be involved in the origin of distinct evolutionary innovations in plants and animals. For example, Pseudomonas aeruginosa cells that evolve new highly divergent functions tend to accumulate mutations in recently duplicated genes. Does TFD facilitate access to a wide range of phenotypes through mutation? What is the effect of TFD on developmental bias? Do the effects of TFD depend on the paralogue's position and role within the network? Addressing these and related questions will poise us better to track causal links between TFD and evolutionary patterns.
Modularity, robustness and evolution.
Many biological systems are modular. That is, their interactions occur predominantly within groups of elements and rarely between groups. In modular systems, perturbations of an element are often contained within its module and have few, little or no effects on the rest of the system. It is thus possible to optimize a module without disturbing the functions of other modules. By allowing independent modification of different traits or functions, modularity increases the range of phenotypes that random genetic change can access. For example, the existence of modules for beak width and length may have allowed the evolution of a wide range of beak shapes in the Darwin finches' adaptive radiation.
Our computational studies have shown that modularity arises easily when networks evolve new additional gene activity patterns. Importantly, modularity increases more when gene networks evolve subject to noise in gene expression. Because these conditions also promote the evolution of robustness, a lack of sensitivity to perturbations, it may be that the evolution of modularity and robustness is correlated. Joint evolution of these two properties may help to explain their prevalence in natural gene regulatory networks.
We will consider several questions that evolutionary biology has left unattended. While it is custom to assume that modularity increases evolvability, no study has addressed the details of how it does so. How do developmental biases are distorted by the consolidation of modules? Do phenotypic changes induced by mutation tend to pertain to a single module in modular networks, as biologists often assume? Do such changes in a single module occur in any direction with equal probability? Do other network traits have a significant role in defining the direction of developmental bias? What is the relationship between robustness and modularity in multifunctional networks? Are these two properties prone to evolve jointly?