The VII AMMCS International Conference

Waterloo, Ontario, Canada | August 17-21, 2026

AMMCS 2026 ALife Conference Plenary Speaker

Canalizing dynamics as a network mechanism for collective decision, control, modularity, and abstraction in living systems

Prof. Luis M. Rocha, State University of New York, Binghamton, USA

In biomolecular regulation, canalization (a term coined by Conrad Waddington to refer to the buffering of genetic, epigenetic, and environmental fluctuations) plays a key role in establishing a robust mapping from genotype to phenotype in noisy environments. Robustness of sensors to fluctuations, requires collective canalization realized with at least two types of dynamical redundancy: 1) heterogenous, nonlinear effective connectivity, whereby most regulatory inputs have little or no effect on downstream signaling and regulation, and 2) symmetry, whereby groups of inputs are causally equivalent. Biologically, this manifests in several ways, including:  multiple signaling pathways, multiple combinations of transcription factors that bind a gene’s promoter region, and threshold behaviors that allow depletion of one signal to be overcome by overabundance of another. We measure effective connectivity and symmetry in experimentally-validated automata network models of biochemical pathways, and demonstrate that these forms of dynamical redundancy are ubiquitous in regulation and signaling. Indeed, the redundancy found in biological models is much more pronounced than what is expected from random networks, and, as we demonstrate, a major reason for them being much more ordered than what the current criticality hypothesis, or “edge-of-chaos” theory, predicts.  The observed redundancy is furthermore shown to shape the controllability and dynamical modularity of biochemical regulation and signaling networks. We also summarize recent computational evolution experiments showing that the necessity of collective decision in noisy environments---e.g. quorum sensing in bacteria or collective intelligence in societies---leads to the evolution of both types of redundancy. As a practical benefit of these results, we show that the observed widespread redundancy in biochemical regulation facilitates the construction of causal models, such as large-scale digital twins for precision medicine. Finally, we discuss how the observed evolution of redundancy constitutes a “selective loss of detail”, which Howard Pattee argues to be required for emergence of new functions in living systems and abstraction in intelligence, and which, we argue, facilitates explanation and prediction in scientific models.
Luis M. Rocha is the George J. Klir Professor of Systems Science at the Thomas J. Watson College of Engineering and Applied Science (School of Systems Science and Industrial Engineering), Binghamton University (State University of New York), where he leads the Complex Adaptive Systems and Computational Intelligence (CASCI) lab. He is also Visiting Professor and Principal Investigator at the Catolica Biomedical Research Center, where he is he is the Era Chair of the CBeRa project "Strategic Integration of Complex Networks and Systems for Advancing Biomedical Research". The CASCI lab he directs works on complex networks & systems, computational & systems biology, and computational intelligence, focusing on characterizing and understanding multiscale complexity involved in human health and society. Projects range from biomedical informatics to understanding redundancy, robustness, modularity and control in complex networks, collective behavior on the web and in social systems, machine learning, bio-inspired computing, and evolutionary systems. He is committed to interdisciplinary research as detailed in his Formal Corner, training students in various academic programs including the NSF-NRT Interdisciplinary Training in Complex Networks and Systems which he spearheaded at Indiana University. He also enjoys life outside of research with family, culture, music, and DJing, as you can explore in his Informal Corner.