@article{7789, abstract = {During embryonic and postnatal development, organs and tissues grow steadily to achieve their final size at the end of puberty. However, little is known about the cellular dynamics that mediate postnatal growth. By combining in vivo clonal lineage tracing, proliferation kinetics, single-cell transcriptomics, andin vitro micro-pattern experiments, we resolved the cellular dynamics taking place during postnatal skin epidermis expansion. Our data revealed that harmonious growth is engineered by a single population of developmental progenitors presenting a fixed fate imbalance of self-renewing divisions with an ever-decreasing proliferation rate. Single-cell RNA sequencing revealed that epidermal developmental progenitors form a more uniform population compared with adult stem and progenitor cells. Finally, we found that the spatial pattern of cell division orientation is dictated locally by the underlying collagen fiber orientation. Our results uncover a simple design principle of organ growth where progenitors and differentiated cells expand in harmony with their surrounding tissues.}, author = {Dekoninck, Sophie and Hannezo, Edouard B and Sifrim, Alejandro and Miroshnikova, Yekaterina A. and Aragona, Mariaceleste and Malfait, Milan and Gargouri, Souhir and De Neunheuser, Charlotte and Dubois, Christine and Voet, Thierry and Wickström, Sara A. and Simons, Benjamin D. and Blanpain, Cédric}, issn = {10974172}, journal = {Cell}, number = {3}, pages = {604--620.e22}, publisher = {Elsevier}, title = {{Defining the design principles of skin epidermis postnatal growth}}, doi = {10.1016/j.cell.2020.03.015}, volume = {181}, year = {2020}, } @article{8220, abstract = {Understanding to what extent stem cell potential is a cell-intrinsic property or an emergent behavior coming from global tissue dynamics and geometry is a key outstanding question of systems and stem cell biology. Here, we propose a theory of stem cell dynamics as a stochastic competition for access to a spatially localized niche, giving rise to a stochastic conveyor-belt model. Cell divisions produce a steady cellular stream which advects cells away from the niche, while random rearrangements enable cells away from the niche to be favorably repositioned. Importantly, even when assuming that all cells in a tissue are molecularly equivalent, we predict a common (“universal”) functional dependence of the long-term clonal survival probability on distance from the niche, as well as the emergence of a well-defined number of functional stem cells, dependent only on the rate of random movements vs. mitosis-driven advection. We test the predictions of this theory on datasets of pubertal mammary gland tips and embryonic kidney tips, as well as homeostatic intestinal crypts. Importantly, we find good agreement for the predicted functional dependency of the competition as a function of position, and thus functional stem cell number in each organ. This argues for a key role of positional fluctuations in dictating stem cell number and dynamics, and we discuss the applicability of this theory to other settings.}, author = {Corominas-Murtra, Bernat and Scheele, Colinda L.G.J. and Kishi, Kasumi and Ellenbroek, Saskia I.J. and Simons, Benjamin D. and Van Rheenen, Jacco and Hannezo, Edouard B}, issn = {10916490}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, number = {29}, pages = {16969--16975}, publisher = {National Academy of Sciences}, title = {{Stem cell lineage survival as a noisy competition for niche access}}, doi = {10.1073/pnas.1921205117}, volume = {117}, year = {2020}, } @article{8669, abstract = {Pancreatic islets play an essential role in regulating blood glucose level. Although the molecular pathways underlying islet cell differentiation are beginning to be resolved, the cellular basis of islet morphogenesis and fate allocation remain unclear. By combining unbiased and targeted lineage tracing, we address the events leading to islet formation in the mouse. From the statistical analysis of clones induced at multiple embryonic timepoints, here we show that, during the secondary transition, islet formation involves the aggregation of multiple equipotent endocrine progenitors that transition from a phase of stochastic amplification by cell division into a phase of sublineage restriction and limited islet fission. Together, these results explain quantitatively the heterogeneous size distribution and degree of polyclonality of maturing islets, as well as dispersion of progenitors within and between islets. Further, our results show that, during the secondary transition, α- and β-cells are generated in a contemporary manner. Together, these findings provide insight into the cellular basis of islet development.}, author = {Sznurkowska, Magdalena K. and Hannezo, Edouard B and Azzarelli, Roberta and Chatzeli, Lemonia and Ikeda, Tatsuro and Yoshida, Shosei and Philpott, Anna and Simons, Benjamin D}, issn = {20411723}, journal = {Nature Communications}, publisher = {Springer Nature}, title = {{Tracing the cellular basis of islet specification in mouse pancreas}}, doi = {10.1038/s41467-020-18837-3}, volume = {11}, year = {2020}, } @article{8672, abstract = {Cell fate transitions are key to development and homeostasis. It is thus essential to understand the cellular mechanisms controlling fate transitions. Cell division has been implicated in fate decisions in many stem cell types, including neuronal and epithelial progenitors. In other stem cells, such as embryonic stem (ES) cells, the role of division remains unclear. Here, we show that exit from naive pluripotency in mouse ES cells generally occurs after a division. We further show that exit timing is strongly correlated between sister cells, which remain connected by cytoplasmic bridges long after division, and that bridge abscission progressively accelerates as cells exit naive pluripotency. Finally, interfering with abscission impairs naive pluripotency exit, and artificially inducing abscission accelerates it. Altogether, our data indicate that a switch in the division machinery leading to faster abscission regulates pluripotency exit. Our study identifies abscission as a key cellular process coupling cell division to fate transitions.}, author = {Chaigne, Agathe and Labouesse, Céline and White, Ian J. and Agnew, Meghan and Hannezo, Edouard B and Chalut, Kevin J. and Paluch, Ewa K.}, issn = {18781551}, journal = {Developmental Cell}, number = {2}, pages = {195--208}, publisher = {Elsevier}, title = {{Abscission couples cell division to embryonic stem cell fate}}, doi = {10.1016/j.devcel.2020.09.001}, volume = {55}, year = {2020}, } @article{7166, abstract = {In the living cell, we encounter a large variety of motile processes such as organelle transport and cytoskeleton remodeling. These processes are driven by motor proteins that generate force by transducing chemical free energy into mechanical work. In many cases, the molecular motors work in teams to collectively generate larger forces. Recent optical trapping experiments on small teams of cytoskeletal motors indicated that the collectively generated force increases with the size of the motor team but that this increase depends on the motor type and on whether the motors are studied in vitro or in vivo. Here, we use the theory of stochastic processes to describe the motion of N motors in a stationary optical trap and to compute the N-dependence of the collectively generated forces. We consider six distinct motor types, two kinesins, two dyneins, and two myosins. We show that the force increases always linearly with N but with a prefactor that depends on the performance of the single motor. Surprisingly, this prefactor increases for weaker motors with a lower stall force. This counter-intuitive behavior reflects the increased probability with which stronger motors detach from the filament during strain generation. Our theoretical results are in quantitative agreement with experimental data on small teams of kinesin-1 motors.}, author = {Ucar, Mehmet C and Lipowsky, Reinhard}, issn = {1530-6992}, journal = {Nano Letters}, number = {1}, pages = {669--676}, publisher = {American Chemical Society}, title = {{Collective force generation by molecular motors is determined by strain-induced unbinding}}, doi = {10.1021/acs.nanolett.9b04445}, volume = {20}, year = {2020}, } @article{7431, abstract = {In many real-world systems, information can be transmitted in two qualitatively different ways: by copying or by transformation. Copying occurs when messages are transmitted without modification, e.g. when an offspring receives an unaltered copy of a gene from its parent. Transformation occurs when messages are modified systematically during transmission, e.g. when mutational biases occur during genetic replication. Standard information-theoretic measures do not distinguish these two modes of information transfer, although they may reflect different mechanisms and have different functional consequences. Starting from a few simple axioms, we derive a decomposition of mutual information into the information transmitted by copying versus the information transmitted by transformation. We begin with a decomposition that applies when the source and destination of the channel have the same set of messages and a notion of message identity exists. We then generalize our decomposition to other kinds of channels, which can involve different source and destination sets and broader notions of similarity. In addition, we show that copy information can be interpreted as the minimal work needed by a physical copying process, which is relevant for understanding the physics of replication. We use the proposed decomposition to explore a model of amino acid substitution rates. Our results apply to any system in which the fidelity of copying, rather than simple predictability, is of critical relevance.}, author = {Kolchinsky, Artemy and Corominas-Murtra, Bernat}, issn = {17425662}, journal = {Journal of the Royal Society Interface}, number = {162}, publisher = {The Royal Society}, title = {{Decomposing information into copying versus transformation}}, doi = {10.1098/rsif.2019.0623}, volume = {17}, year = {2020}, } @misc{9885, abstract = {Data obtained from the fine-grained simulations used in Figures 2-5, data obtained from the coarse-grained numerical calculations used in Figure 6, and a sample script for the fine-grained simulation as a Jupyter notebook (ZIP)}, author = {Ucar, Mehmet C and Lipowsky, Reinhard}, publisher = {American Chemical Society }, title = {{MURL_Dataz}}, doi = {10.1021/acs.nanolett.9b04445.s002}, year = {2020}, } @article{6832, abstract = {Steady-state turnover is a hallmark of epithelial tissues throughout adult life. Intestinal epithelial turnover is marked by continuous cell migration, which is assumed to be driven by mitotic pressure from the crypts. However, the balance of forces in renewal remains ill-defined. Combining biophysical modeling and quantitative three-dimensional tissue imaging with genetic and physical manipulations, we revealed the existence of an actin-related protein 2/3 complex–dependent active migratory force, which explains quantitatively the profiles of cell speed, density, and tissue tension along the villi. Cells migrate collectively with minimal rearrangements while displaying dual—apicobasal and front-back—polarity characterized by actin-rich basal protrusions oriented in the direction of migration. We propose that active migration is a critical component of gut epithelial turnover.}, author = {Krndija, Denis and Marjou, Fatima El and Guirao, Boris and Richon, Sophie and Leroy, Olivier and Bellaiche, Yohanns and Hannezo, Edouard B and Vignjevic, Danijela Matic}, journal = {Science}, number = {6454}, pages = {705--710}, publisher = {American Association for the Advancement of Science}, title = {{Active cell migration is critical for steady-state epithelial turnover in the gut}}, doi = {10.1126/science.aau3429}, volume = {365}, year = {2019}, } @article{5789, abstract = {Tissue morphogenesis is driven by mechanical forces that elicit changes in cell size, shape and motion. The extent by which forces deform tissues critically depends on the rheological properties of the recipient tissue. Yet, whether and how dynamic changes in tissue rheology affect tissue morphogenesis and how they are regulated within the developing organism remain unclear. Here, we show that blastoderm spreading at the onset of zebrafish morphogenesis relies on a rapid, pronounced and spatially patterned tissue fluidization. Blastoderm fluidization is temporally controlled by mitotic cell rounding-dependent cell–cell contact disassembly during the last rounds of cell cleavages. Moreover, fluidization is spatially restricted to the central blastoderm by local activation of non-canonical Wnt signalling within the blastoderm margin, increasing cell cohesion and thereby counteracting the effect of mitotic rounding on contact disassembly. Overall, our results identify a fluidity transition mediated by loss of cell cohesion as a critical regulator of embryo morphogenesis.}, author = {Petridou, Nicoletta and Grigolon, Silvia and Salbreux, Guillaume and Hannezo, Edouard B and Heisenberg, Carl-Philipp J}, issn = {14657392}, journal = {Nature Cell Biology}, pages = {169–178}, publisher = {Nature Publishing Group}, title = {{Fluidization-mediated tissue spreading by mitotic cell rounding and non-canonical Wnt signalling}}, doi = {10.1038/s41556-018-0247-4}, volume = {21}, year = {2019}, } @article{5944, abstract = {Understanding the thermodynamics of the duplication process is a fundamental step towards a comprehensive physical theory of biological systems. However, the immense complexity of real cells obscures the fundamental tensions between energy gradients and entropic contributions that underlie duplication. The study of synthetic, feasible systems reproducing part of the key ingredients of living entities but overcoming major sources of biological complexity is of great relevance to deepen the comprehension of the fundamental thermodynamic processes underlying life and its prevalence. In this paper an abstract—yet realistic—synthetic system made of small synthetic protocell aggregates is studied in detail. A fundamental relation between free energy and entropic gradients is derived for a general, non-equilibrium scenario, setting the thermodynamic conditions for the occurrence and prevalence of duplication phenomena. This relation sets explicitly how the energy gradients invested in creating and maintaining structural—and eventually, functional—elements of the system must always compensate the entropic gradients, whose contributions come from changes in the translational, configurational, and macrostate entropies, as well as from dissipation due to irreversible transitions. Work/energy relations are also derived, defining lower bounds on the energy required for the duplication event to take place. A specific example including real ternary emulsions is provided in order to grasp the orders of magnitude involved in the problem. It is found that the minimal work invested over the system to trigger a duplication event is around ~ 10−13J , which results, in the case of duplication of all the vesicles contained in a liter of emulsion, in an amount of energy around ~ 1kJ . Without aiming to describe a truly biological process of duplication, this theoretical contribution seeks to explicitly define and identify the key actors that participate in it.}, author = {Corominas-Murtra, Bernat}, issn = {20751729}, journal = {Life}, number = {1}, publisher = {MDPI}, title = {{Thermodynamics of duplication thresholds in synthetic protocell systems}}, doi = {10.3390/life9010009}, volume = {9}, year = {2019}, } @article{6191, abstract = {The formation of self-organized patterns is key to the morphogenesis of multicellular organisms, although a comprehensive theory of biological pattern formation is still lacking. Here, we propose a minimal model combining tissue mechanics with morphogen turnover and transport to explore routes to patterning. Our active description couples morphogen reaction and diffusion, which impact cell differentiation and tissue mechanics, to a two-phase poroelastic rheology, where one tissue phase consists of a poroelastic cell network and the other one of a permeating extracellular fluid, which provides a feedback by actively transporting morphogens. While this model encompasses previous theories approximating tissues to inert monophasic media, such as Turing’s reaction–diffusion model, it overcomes some of their key limitations permitting pattern formation via any two-species biochemical kinetics due to mechanically induced cross-diffusion flows. Moreover, we describe a qualitatively different advection-driven Keller–Segel instability which allows for the formation of patterns with a single morphogen and whose fundamental mode pattern robustly scales with tissue size. We discuss the potential relevance of these findings for tissue morphogenesis.}, author = {Recho, Pierre and Hallou, Adrien and Hannezo, Edouard B}, issn = {10916490}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, number = {12}, pages = {5344--5349}, publisher = {National Academy of Sciences}, title = {{Theory of mechanochemical patterning in biphasic biological tissues}}, doi = {10.1073/pnas.1813255116}, volume = {116}, year = {2019}, } @article{6508, abstract = {Segregation of maternal determinants within the oocyte constitutes the first step in embryo patterning. In zebrafish oocytes, extensive ooplasmic streaming leads to the segregation of ooplasm from yolk granules along the animal-vegetal axis of the oocyte. Here, we show that this process does not rely on cortical actin reorganization, as previously thought, but instead on a cell-cycle-dependent bulk actin polymerization wave traveling from the animal to the vegetal pole of the oocyte. This wave functions in segregation by both pulling ooplasm animally and pushing yolk granules vegetally. Using biophysical experimentation and theory, we show that ooplasm pulling is mediated by bulk actin network flows exerting friction forces on the ooplasm, while yolk granule pushing is achieved by a mechanism closely resembling actin comet formation on yolk granules. Our study defines a novel role of cell-cycle-controlled bulk actin polymerization waves in oocyte polarization via ooplasmic segregation.}, author = {Shamipour, Shayan and Kardos, Roland and Xue, Shi-lei and Hof, Björn and Hannezo, Edouard B and Heisenberg, Carl-Philipp J}, issn = {10974172}, journal = {Cell}, number = {6}, pages = {1463--1479.e18}, publisher = {Elsevier}, title = {{Bulk actin dynamics drive phase segregation in zebrafish oocytes}}, doi = {10.1016/j.cell.2019.04.030}, volume = {177}, year = {2019}, } @article{6513, abstract = {Adult intestinal stem cells are located at the bottom of crypts of Lieberkühn, where they express markers such as LGR5 1,2 and fuel the constant replenishment of the intestinal epithelium1. Although fetal LGR5-expressing cells can give rise to adult intestinal stem cells3,4, it remains unclear whether this population in the patterned epithelium represents unique intestinal stem-cell precursors. Here we show, using unbiased quantitative lineage-tracing approaches, biophysical modelling and intestinal transplantation, that all cells of the mouse intestinal epithelium—irrespective of their location and pattern of LGR5 expression in the fetal gut tube—contribute actively to the adult intestinal stem cell pool. Using 3D imaging, we find that during fetal development the villus undergoes gross remodelling and fission. This brings epithelial cells from the non-proliferative villus into the proliferative intervillus region, which enables them to contribute to the adult stem-cell niche. Our results demonstrate that large-scale remodelling of the intestinal wall and cell-fate specification are closely linked. Moreover, these findings provide a direct link between the observed plasticity and cellular reprogramming of differentiating cells in adult tissues following damage5,6,7,8,9, revealing that stem-cell identity is an induced rather than a hardwired property.}, author = {Guiu, Jordi and Hannezo, Edouard B and Yui, Shiro and Demharter, Samuel and Ulyanchenko, Svetlana and Maimets, Martti and Jørgensen, Anne and Perlman, Signe and Lundvall, Lene and Mamsen, Linn Salto and Larsen, Agnete and Olesen, Rasmus H. and Andersen, Claus Yding and Thuesen, Lea Langhoff and Hare, Kristine Juul and Pers, Tune H. and Khodosevich, Konstantin and Simons, Benjamin D. and Jensen, Kim B.}, issn = {14764687}, journal = {Nature}, pages = {107--111}, publisher = {Springer Nature}, title = {{Tracing the origin of adult intestinal stem cells}}, doi = {10.1038/s41586-019-1212-5}, volume = {570}, year = {2019}, } @article{6559, abstract = {Branching morphogenesis is a prototypical example of complex three-dimensional organ sculpting, required in multiple developmental settings to maximize the area of exchange surfaces. It requires, in particular, the coordinated growth of different cell types together with complex patterning to lead to robust macroscopic outputs. In recent years, novel multiscale quantitative biology approaches, together with biophysical modelling, have begun to shed new light of this topic. Here, we wish to review some of these recent developments, highlighting the generic design principles that can be abstracted across different branched organs, as well as the implications for the broader fields of stem cell, developmental and systems biology.}, author = {Hannezo, Edouard B and Simons, Benjamin D.}, issn = {18790410}, journal = {Current Opinion in Cell Biology}, pages = {99--105}, publisher = {Elsevier}, title = {{Multiscale dynamics of branching morphogenesis}}, doi = {10.1016/j.ceb.2019.04.008}, volume = {60}, year = {2019}, } @article{6601, abstract = {There is increasing evidence that both mechanical and biochemical signals play important roles in development and disease. The development of complex organisms, in particular, has been proposed to rely on the feedback between mechanical and biochemical patterning events. This feedback occurs at the molecular level via mechanosensation but can also arise as an emergent property of the system at the cellular and tissue level. In recent years, dynamic changes in tissue geometry, flow, rheology, and cell fate specification have emerged as key platforms of mechanochemical feedback loops in multiple processes. Here, we review recent experimental and theoretical advances in understanding how these feedbacks function in development and disease.}, author = {Hannezo, Edouard B and Heisenberg, Carl-Philipp J}, issn = {00928674}, journal = {Cell}, number = {1}, pages = {12--25}, publisher = {Elsevier}, title = {{Mechanochemical feedback loops in development and disease}}, doi = {10.1016/j.cell.2019.05.052}, volume = {178}, year = {2019}, } @misc{9726, abstract = {A detailed description of the two stochastic models, table of parameters, supplementary data for Figures 4 and 5, parameter dependence of the results, and an analysis on motors with different force–velocity functions (PDF)}, author = {Ucar, Mehmet C and Lipowsky, Reinhard}, publisher = {American Chemical Society }, title = {{Supplementary information - Collective force generation by molecular motors is determined by strain-induced unbinding}}, doi = {10.1021/acs.nanolett.9b04445.s001}, year = {2019}, } @article{288, abstract = {Recent lineage tracing studies have revealed that mammary gland homeostasis relies on unipotent stem cells. However, whether and when lineage restriction occurs during embryonic mammary development, and which signals orchestrate cell fate specification, remain unknown. Using a combination of in vivo clonal analysis with whole mount immunofluorescence and mathematical modelling of clonal dynamics, we found that embryonic multipotent mammary cells become lineage-restricted surprisingly early in development, with evidence for unipotency as early as E12.5 and no statistically discernable bipotency after E15.5. To gain insights into the mechanisms governing the switch from multipotency to unipotency, we used gain-of-function Notch1 mice and demonstrated that Notch activation cell autonomously dictates luminal cell fate specification to both embryonic and basally committed mammary cells. These functional studies have important implications for understanding the signals underlying cell plasticity and serve to clarify how reactivation of embryonic programs in adult cells can lead to cancer.}, author = {Lilja, Anna and Rodilla, Veronica and Huyghe, Mathilde and Hannezo, Edouard B and Landragin, Camille and Renaud, Olivier and Leroy, Olivier and Rulands, Steffen and Simons, Benjamin and Fré, Silvia}, journal = {Nature Cell Biology}, number = {6}, pages = {677 -- 687}, publisher = {Nature Publishing Group}, title = {{Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland}}, doi = {10.1038/s41556-018-0108-1}, volume = {20}, year = {2018}, } @article{3, abstract = {SETD5 gene mutations have been identified as a frequent cause of idiopathic intellectual disability. Here we show that Setd5-haploinsufficient mice present developmental defects such as abnormal brain-to-body weight ratios and neural crest defect-associated phenotypes. Furthermore, Setd5-mutant mice show impairments in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile of ultrasonic vocalization, and behavioral inflexibility. Behavioral issues are accompanied by abnormal expression of postsynaptic density proteins previously associated with cognition. Our data additionally indicate that Setd5 regulates RNA polymerase II dynamics and gene transcription via its interaction with the Hdac3 and Paf1 complexes, findings potentially explaining the gene expression defects observed in Setd5-haploinsufficient mice. Our results emphasize the decisive role of Setd5 in a biological pathway found to be disrupted in humans with intellectual disability and autism spectrum disorder.}, author = {Deliu, Elena and Arecco, Niccoló and Morandell, Jasmin and Dotter, Christoph and Contreras, Ximena and Girardot, Charles and Käsper, Eva and Kozlova, Alena and Kishi, Kasumi and Chiaradia, Ilaria and Noh, Kyung and Novarino, Gaia}, journal = {Nature Neuroscience}, number = {12}, pages = {1717 -- 1727}, publisher = {Nature Publishing Group}, title = {{Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition}}, doi = {10.1038/s41593-018-0266-2}, volume = {21}, year = {2018}, } @article{5787, abstract = {Branching morphogenesis remains a subject of abiding interest. Although much is known about the gene regulatory programs and signaling pathways that operate at the cellular scale, it has remained unclear how the macroscopic features of branched organs, including their size, network topology and spatial patterning, are encoded. Lately, it has been proposed that, these features can be explained quantitatively in several organs within a single unifying framework. Based on large- scale organ recon - structions and cell lineage tracing, it has been argued that morphogenesis follows from the collective dynamics of sublineage- restricted self- renewing progenitor cells, localized at ductal tips, that act cooperatively to drive a serial process of ductal elon - gation and stochastic tip bifurcation. By correlating differentiation or cell cycle exit with proximity to maturing ducts, this dynamic results in the specification of a com- plex network of defined density and statistical organization. These results suggest that, for several mammalian tissues, branched epithelial structures develop as a self- organized process, reliant upon a strikingly simple, but generic, set of local rules, without recourse to a rigid and deterministic sequence of genetically programmed events. Here, we review the basis of these findings and discuss their implications.}, author = {Hannezo, Edouard B and Simons, Benjamin D.}, issn = {00121592}, journal = {Development Growth and Differentiation}, number = {9}, pages = {512--521}, publisher = {Wiley}, title = {{Statistical theory of branching morphogenesis}}, doi = {10.1111/dgd.12570}, volume = {60}, year = {2018}, } @article{5859, abstract = {The emergence of syntax during childhood is a remarkable example of how complex correlations unfold in nonlinear ways through development. In particular, rapid transitions seem to occur as children reach the age of two, which seems to separate a two-word, tree-like network of syntactic relations among words from the scale-free graphs associated with the adult, complex grammar. Here, we explore the evolution of syntax networks through language acquisition using the chromatic number, which captures the transition and provides a natural link to standard theories on syntactic structures. The data analysis is compared to a null model of network growth dynamics which is shown to display non-trivial and sensible differences. At a more general level, we observe that the chromatic classes define independent regions of the graph, and thus, can be interpreted as the footprints of incompatibility relations, somewhat as opposed to modularity considerations.}, author = {Corominas-Murtra, Bernat and Fibla, Martí Sànchez and Valverde, Sergi and Solé, Ricard}, issn = {2054-5703}, journal = {Royal Society Open Science}, number = {12}, publisher = {The Royal Society}, title = {{Chromatic transitions in the emergence of syntax networks}}, doi = {10.1098/rsos.181286}, volume = {5}, year = {2018}, }