Ricard V. Solé

This study shows that sessile and mobile cognitive strategies evolve as alternative solutions to foraging in uncertain environments, depending on resource return structures and ecological feedbacks.

This study develops a computational framework to model genomic instability in tumors, showing it can both drive evolution and lead to population collapse, with implications for therapy.

This study investigates the effects of synthetic horizontal gene transfer in ecological consortia models to promote biodiversity and regulate gene propagation.

The paper introduces a dynamical model to study how gut virome influences microbiome recovery after antibiotic-induced dysbiosis, identifying ecological thresholds and a firewall mechanism for pathogen suppression.

The paper develops a theoretical framework to assess the invasion potential of mirror life in ecosystems, showing ecological constraints limit its establishment.

This paper develops a geometric framework to show how energetic constraints shape ecological network diversity, revealing a unimodal relationship between energy supply and biodiversity.

This paper designs synthetic genetic circuits to implement non-associative learning behaviors in unicellular and multicellular systems.

The paper shows metabolic scaling diversity arises from stochastic cellular growth dynamics, not fixed mass-metabolism relationships.

This paper designs and evaluates minimal genetic circuits that enable cells to anticipate environmental trends through deterministic and stochastic analyses.

The paper links power, efficiency, and bifurcations in consumer-resource systems using mathematical models and shows how ecological principles can be formalized and tested.

The paper shows that ecological systems develop in a sequenced order from fast-to slow-growing taxa due to environmental resistance minimization, supported by theoretical and empirical evidence.

The paper models tumors as ecological communities using the Generalized Lotka-Volterra model to understand intra-tumor heterogeneity and its implications for cancer progression and treatment resistance.

The paper designs synthetic genetic circuits in E. coli to demonstrate Turing pattern formation through an activator-inhibitor mechanism.

The paper presents a mathematical model to explore the relationship between tumor genetic instability and immune response, showing that increased mutational load and immune migration can lead to cancer clearance.

The paper shows that toxic environments with resource-waste dynamics promote cellular diversity through metabolic tradeoffs and spatial interactions.

This paper explores the collective dynamics, memory, and learning properties of liquid brains using statistical physics, comparing them to solid brains, ant colonies, and the immune system.

The paper develops mathematical models for four synthetic Terraformation motifs to understand their stability and effectiveness in preventing ecosystem collapse.