arXiv subjects

Hossein Nemati

Publications and source records attributed to Hossein Nemati.

4 recordsLinked to original sources

arXiv2026

Genotype specificity and spatial arrangement govern the direction and magnitude of selection in variable environments

Spatial environmental variation can either amplify or suppress the fixation of beneficial mutants in structured populations, yet the interplay of ecological factors and spatial structure in determining which outcome occurs remains theoretically unresolved. Here, we develop a unified framework for selection on lattice graphs with environmental heterogeneity, in which mutant and resident fitness depend on the local environmental state. Across three common classes of genotype-environment interactions and a wide range of spatial arrangements of environmental states, we identify two governing principles. Genotype specificity determines the direction of the effect: heterogeneity amplifies selection when it modulates resident fitness, but suppresses selection when it modulates mutant fitness, with genotype-symmetric modulation producing weaker amplification. Spatial arrangement determines the magnitude: intermixed versus clustered environments tune the strength of amplification or suppression without reversing the direction of the effect. Together, these principles reconcile disparate theoretical results and provide predictive criteria for adaptation in heterogeneous landscapes, from microbial communities to somatic evolution and cancer.

q-bio.PE↗

arXiv2025

Cell Competition Driven by Secreted Ligands: Modeling Liver Metastasis of Colorectal Cancer

Cell competition in multicellular organisms has been shown to play a critical role during the development of organisms, cancer progression, and in the establishment and maintenance of tissue homeostasis. Various mechanisms of cell competition have been identified, including active elimination via mechanical forces or induced apoptosis, as well as competition for nutrients and other beneficial factors. A recent experiment demonstrated hallmarks of cell competition, associated with cell cycle dynamics, between liver progenitor cells and colorectal cancer cells [Krotenberg Garcia et al., iScience 27, 109718 (2024)]. However, a mechanistic explanation for this form of competition remains lacking. Here, we present a mean-field model of competition for signaling ligands, coupled with cell cycle dynamics, to provide such an understanding. Our model captures the salient features of the experiment, including population dynamics and cell cycle variations. We demonstrate that secretion of a beneficial factor by cells, coupled with the enhanced uptake efficiency of cancer cells, suffices to reproduce the experimental outcome. Our model, reminiscent of competition for secreted growth factors, provides insight into the minimal level of complexity required to achieve the observed competitive outcome as well as its link to cell cycle dynamics. It can also serve as a general framework for studying biological populations with growth-stage-dependent competition over consumer-produced products.

physics.bio-ph↗

arXiv2024

The Cellular Potts Model on Disordered Lattices

The Cellular Potts model, also known as the Glazier-Graner-Hogeweg model, is a lattice-based approach by which biological tissues at the level of individual cells can be numerically studied. Traditionally, a square or hexagonal underlying lattice structure is assumed for two-dimensional systems, and this is known to introduce artifacts in the structure and dynamics of the model tissues. That is, on regular lattices, cells can assume shapes that are dictated by the symmetries of the underlying lattice. Here, we developed a variant of this method that can be applied to a broad class of (ir)regular lattices. We show that on an irregular lattice deriving from a fluid-like configuration, two types of artifacts can be removed. We further report on the transition between a fluid-like disordered and a solid-like hexagonally ordered phase present for monodisperse confluent cells as a function of their surface tension. This transition shows the hallmarks of a first-order phase transition and is different from the glass/jamming transitions commonly reported for the vertex and active Voronoi models. We emphasize this by analyzing the distribution of shape parameters found in our state space. Our analysis provides a useful reference for the future study of epithelia using the (ir)regular Cellular Potts model.

cond-mat.soft↗

arXiv2022

Counterintuitive properties of fixation probability and fixation time in population structures with spatially periodic resource distribution

Resource are often not uniformly distributed within a population. Spatial variations of concentration of a resource, change the fitness of competing strategies locally. The notion of fitness varying with respect to both genotype and environment is important in modeling cancer initiation, microbial evolution and evolution of drug resistance. Environmental interactions can be asymmetric, that is, they affect the fitness of one type more than the other. The question is how local environmental variations in network population structures change the selection dynamics in a finite population setting. We consider one-dimensional lattice population structures with spatial fitness distributions with a periodic pattern. Heterogeneity is determined by standard deviation of fitnesses and period. The model covers biologically relevant limits of two-habitat subdivided populations and randomly-distributed resources in high- and low-periods. We numerically calculate fixation probability and fixation times for a constant population birth-death process as fitness heterogeneity and period vary. We identify levels of heterogeneity for which a previously deleterious mutant, in a uniform environment, becomes beneficial. In other regimes of the problem we observe unexpected behavior where the fixation probability of both types are larger than their neutral value at the same time. This coincides with an exponential increase in time to fixation as a function of population size, which points to significant slow-down in selection process and the potential for coexistence between types in realistic time scales. We also discuss `fitness shift' model where the fitness function of one type is identical to the other up to a constant spatial shift. This leads to significant increase (or decrease) in the fixation probability of the mutant depending the value of the shift.

q-bio.PE↗