Biology subjects

Colizzi, E. S.

Publications and source records attributed to Colizzi, E. S..

5 recordsLinked to original sources

bioRxiv2026

Regulatory architecture tunes gene expression noise in the plant heat shock response

Cells within the same tissue can respond differently to the same stress, yet how gene regulatory networks generate and control this variability remains unclear. Here, we show that cell-to-cell variation in the Arabidopsis heat shock response is coordinated across the heat shock regulon and that the distribution of responses is tuned by the underlying regulatory network. Imaging of an HSP70 promoter reporter revealed basal activity in a subset of root cells and heterogeneous induction after heat shock, with some cells remaining near pre-stress expression levels. Dual reporters showed strong coordination between independently integrated HSP70 reporter loci, consistent with substantial shared upstream regulatory variation. Single-nucleus RNA sequencing confirmed heterogeneous but coordinated activation of heat shock genes across root cell types. Stronger heat shock states at both ambient and heat stress temperatures were associated with a recurrent thermoprotective programme across root cell populations, whereas weak responders after heat shock were associated with distinct cell-type specific transcriptional programmes, including defence- and jasmonate-associated states in some root cell types. Stochastic modelling suggested that HSFA2-dependent amplification could broaden the distribution of HSP70 expression across cells. Consistent with this prediction, experiments showed that loss of HSFA2 reduced HSP70 induction and lowered cell-to-cell variability after controlling for differences in mean expression. Together, these results show that the plant heat shock network controls both the magnitude and distribution of stress-responsive gene expression across cells.

plant biology↗

bioRxiv2025

Evolution of reproduction driven by ecology at the onset of multicellularity

At the origin of multicellularity, genetic programs used by single-celled organisms to interact with their environment become organised into a developmental program. While previous work has clarified the selective advantages of simple multicellularity, the origin of development remains unclear. Here, we investigate the ecological origin of a fundamental developmental process -- multicellular reproduction -- using a computational model where cells forage in a structured environment, and evolve adhesion and regulated environmental responses. Multicellular modes of reproduction are not pre-specified in the model, but must emerge from the evolving dynamics under ecological selection. We find that distinct multicellular life cycles evolve depending on the spatial distribution of resources. Among these are life cycles with a single-celled propagule phase the most prevalent reproductive strategy in multicellular life that evolves as a dispersal strategy to reach new resources. These propagules form through the activation of molecular programs co-opted from the unicellular ancestor, where they mediated interactions with neighbours in its ecological context. Once propagules evolve, multicellular lineages can invade environments previously dominated by unicellular competitors, showing this strategy is adaptive beyond the conditions that permit its evolution. Altogether, our results show that developmental regulation evolves through co-option of ecological interactions during the transition to multicellularity. Significance statementReproduction is a universal feature of life. Yet, the evolution of multicellularity transformed it fundamentally: while single-celled organisms reproduce via cell division, reproduction in multicellular organisms is a complex process involving the coordination of many cells. How these new forms of multicellular reproduction first evolved is currently unknown. Using a computational model, we study how group reproduction emerges from the collective dynamics of individual cells. The model shows that unicellular ancestral life cycles can be repurposed as propagules used for reproduction in multicellular species, suggesting that genetic co-option is a key mechanism through which early development evolves.

evolutionary biology↗

bioRxiv2022

Evolution of selfish multicellularity: collective organisation of individual spatio-temporal regulatory strategies

BackgroundThe unicellular ancestors of modern-day multicellular organisms were remarkably complex. They had an extensive set of regulatory and signalling genes, an intricate life cycle and could change their behaviour in response to environmental changes. At the transition to multicellularity, some of these behaviours were co-opted to organise the development of the nascent multicellular organism. Here, we focus on the transition to multicellularity before the evolution of stable cell differentiation, to reveal how the emergence of clusters affects the evolution of cell behaviour. ResultsWe construct a computational model of a population of cells that can evolve the regulation of their behavioural state - either division or migration - in a unicellular or multicellular context. They compete for reproduction and for resources to survive in a seasonally changing environment. We find that the evolution of multicellularity strongly determines the co-evolution of cell behaviour, by altering the competition dynamics between cells. When adhesion cannot evolve, cells compete for survival by rapidly migrating towards resources before dividing. When adhesion evolves, emergent collective migration alleviates the pressure on individual cells to reach resources. This allows cells to selfishly maximise replication. Migrating adhesive clusters display striking patterns of spatio-temporal cell state changes that visually resemble animal development. ConclusionsOur model demonstrates how emergent selection pressures at the onset of multicellularity can drive the evolution of cellular behaviour to give rise to developmental patterns.

evolutionary biology↗

bioRxiv2021

Evolution of genome fragility enables microbial division of labor

Division of labor can evolve when social groups benefit from the functional specialization of its members. Recently, a novel means of coordinating division of labor was found in the antibiotic-producing bacterium Streptomyces coelicolor, where functionally specialized cells are generated through large-scale genomic re-organization. Here, we investigate how the evolution of a genome architecture enables such mutation-driven division of labor, using a multi-scale mathematical model of bacterial evolution. We let bacteria compete on the basis of their antibiotic production and growth rate in a spatially structured environment. Bacterial behavior is determined by the structure and composition of their genome, which encodes antibiotics, growth-promoting genes and fragile genomic loci that can induce chromosomal deletions. We find that a genomic organization evolves that partitions growth-promoting genes and antibiotic-coding genes to distinct parts of the genome, separated by fragile genomic loci. Mutations caused by these fragile sites mostly delete growth-promoting genes, generating antibiotic-producing mutants from non-producing (and weakly-producing) progenitors, in agreement with experimental observations. Mutants protect their colony from competitors but are themselves unable to replicate. We further show that this division of labor enhances the local competition between colonies by promoting antibiotic diversity. These results show that genomic organization can co-evolve with genomic instabilities to enable reproductive division of labor. Motivation of current workDivision of labor can evolve if trade-offs are present between different traits. To organize a division of labor, the genome architecture must evolve to enable differentiated cellular phenotypes. Cell differentiation may be coordinated through gene regulation, as occurs during embryonic development. Alternatively, when mutation rates are high, mutations themselves can guide cell and functional differentiation; however, how this evolves and is organized at the genome level remains unclear. Here, using a model of antibiotic-producing bacteria based on multicellular Streptomyces, we show that if antibiotic production trades off with replication, genome architecture can evolve to support a mutation-driven division of labor. These results are consistent with recent experimental observations and may underlie division of labor in many bacterial groups.

evolutionary biology↗

bioRxiv2020

Evolution of multicellularity by collective integration of spatial information

At the origin of multicellularity, cells may have evolved aggregation in response to predation, for functional specialisation or to allow large-scale integration of environmental cues. These group-level properties emerged from the interactions between cells in a group, and determined the selection pressures experienced by these cells. We investigate the evolution of multicellularity with an evolutionary model where cells search for resources by chemotaxis in a shallow, noisy gradient. Cells can evolve their adhesion to others in a periodically changing environment, where a cells fitness solely depends on its distance from the gradient source. We show that multicellular aggregates evolve because they perform chemo-taxis more efficiently than single cells. Only when the environment changes too frequently, a unicellular state evolves which relies on cell dispersal. Both strategies prevent the invasion of the other through interference competition, creating evolutionary bi-stability. Therefore, collective behaviour can be an emergent selective driver for undifferentiated multicellularity.

evolutionary biology↗