A major problem in our understanding of how complexity has evolved has to do with the so called genotype-phenotype mapping. In its simplest form, we can definite problem as the highly nonlinear relationship that exists between DNA sequence and the phenotype (at any scale). DNA, the genetic string of nucleotides, defines a first layer of information that needs to be read and decoded by cellular hardware, roughly defined by the large set of proteins and small RNAs, ribosomes and other molecular machines. Such a decoding process is not a simple, linear transformation. Even at the protein level, we cannot simple see proteins as chains that have been translated in a one-to-one way: in order to perform functions, proteins must fold and they usually do their functionalities by interacting with other proteins. Many proteins feedback to DNA, controlling and tuning their own synthesis and the synthesis of others. They also attach to different cellular organelles and structures (such as the membrane) and thus even at this level we can say that the upper-scale functionality cannot be reduced to the original sequence. 

The genotype-phenotype mapping problem becomes much more dramatic as we move into developmental processes. In multicellular organisms, a whole individual -which can be composed by billions of cells- is created by starting from a single cell. Since there is no information in DNA about the location of neurons in our brain, or how an eye gets formed, we must conclude that the original information needs to unfold and interact with newly formed structures in a complex, nonlinear way. How is the sequence mapped into the final form? 


 Selection forces act at the level of the organism (the phenotype) whereas variation occurs at the sequence level (through mutation mainly). The coupling between sequence and form is described by the process of development, which somewhat contains the mapping. Such mapping is a consequence of a number of mechanisms of cell growth, attachment, differentiation, migration and pattern formation (among others). How the first patern-forming programs emerged is one of the great questions that we seek to answer. 




Emergence of multicellularity in a model of cell growth death and aggregation under size-dependent selection. Salva Duran-Nebreda and Ricard V. Solé arXiv preprint arXiv:1404.0196 (2014) Royal Society Interface (submitted)

In silico transitions to multicellularity. Ricard V. Solé and Salva Duran-Nebreda arXiv preprint arXiv:1403.3217 (2014) In: Nedelcu, A.M. and Ruiz-Trillo, I. (eds.) (in press). Evolutionary Transitions to Multicellular Life: Principles and Mechanisms. Springer-Verlag London

Before the Endless Forms: Embodied Model of Transition from Single Cells to Aggregates to Ecosystem Engineering. Ricard V. Solé and Sergi Valverde PloS one, 8(4), e59664 (2013)

Macroevolution in silico: scale, constraints and universals. Ricard V. Solé and Sergi Valverde Paleontology, 56(6), 1327-1340. (2013)

Evolved Modular Epistasis in Artificial Organisms. Sergi Valverde, Ricard V. Solé and Santiago Elena Artificial Life, 13, 111-115 (2012)

The causes of epistasis in genetic networks. Javier Macía, Ricard V. Solé and Santiago Elena Evolution, 66(2), 586-596

Distributed robustness in cellular networks: insights from synthetic evolved circuits. Javier Macía and Ricard V. Solé. Journal of The Royal Society Interface, 6(33), 393-400 (2009) 

Neutrality and Robustness in Evo-Devo: Emergence of Lateral Inhibition. Andreea Munteanu and Ricard V. Solé PLoS computational biology, 4(11), e1000226 (2008) 

Neutral fitness landscapes in signalling networks. Pau Fernández and Ricard V. Solé Journal of The Royal Society Interface, 4(12), 41-47 (2007) 

Adaptive walks in a gene network model of morphogenesis: insights into the Cambrian explosion. Ricard V. Solé, Pau Fernández and Stuart A. Kauffman Int J Dev Biol 47(7-8), 685-693 (2003) 

Common Pattern Formation, Modularity and Phase Transitions in a Gene Network Model of Morphogenesis.  Ricard V. Solé, Isaac Salazar-Ciudad and Jordi García-Fernández Physica A: Statistical Mechanics and its Applications, 305(3-4), 640-654 (2002)