Clonal dynamics of surface-driven growing tissues.

The self-organization of cells into complex tissues relies on a tight coordination of cell behavior. Identifying the cellular processes driving tissue growth is key to understanding the emergence of tissue forms and devising targeted therapies for aberrant growth, such as in cancer. Inferring the mode of tissue growth, whether it is driven by cells on the surface or by cells in the bulk, is possible in cell culture experiments but difficult in most tissues in living organisms (in vivo). Genetic tracing experiments, where a subset of cells is labeled with inheritable markers, have become important experimental tools to study cell fate in vivo. Here we show that the mode of tissue growth is reflected in the size distribution of the progeny of marked cells. To this end, we derive the clone size distributions using analytical calculations in the limit of negligible cell migration and cell death, and we test our predictions with an agent-based stochastic sampling technique. We show that for surface-driven growth the clone size distribution takes a characteristic power-law form with an exponent determined by fluctuations of the tissue surface. Our results propose a possible way of determining the mode of tissue growth from genetic tracing experiments.

Accounting for endogenous effects in decision-making with a non-linear diffusion decision model.

The Drift-Diffusion Model (DDM) is widely accepted for two-alternative forced-choice decision paradigms thanks to its simple formalism and close fit to behavioral and neurophysiological data. However, this formalism presents strong limitations in capturing inter-trial dynamics at the single-trial level and endogenous influences. We propose a novel model, the non-linear Drift-Diffusion Model (nl-DDM), that addresses these issues by allowing the existence of several trajectories to the decision boundary. We show that the non-linear model performs better than the drift-diffusion model for an equivalent complexity. To give better intuition on the meaning of nl-DDM parameters, we compare the DDM and the nl-DDM through correlation analysis. This paper provides evidence of the functioning of our model as an extension of the DDM. Moreover, we show that the nl-DDM captures time effects better than the DDM. Our model paves the way toward more accurately analyzing across-trial variability for perceptual decisions and accounts for peri-stimulus influences.