bioRxiv Science⌕ Search

bioRxiv · 10.1101/533133

Testing models of mRNA localization reveals robustness regulated by reducing transport between cells

Abstract

Robust control of gene expression in both space and time is of central importance in the regulation of cellular processes, and for multicellular development. However, the mechanisms by which robustness is achieved are generally not identified or well understood. For example, mRNA localization by molecular-motor-driven transport is crucial for cell polarization in numerous contexts, but the regulatory mechanisms that enable this process to take place in the face of noise or significant perturbations are not fully understood. Here we use a combined experimental-theoretical approach to characterize the robustness of gurken/TGF-alpha mRNA localization in Drosophila egg chambers, where the oocyte and 15 surrounding nurse cells are connected in a stereotypic network via intracellular bridges known as ring canals. We construct a mathematical model that encodes simplified descriptions of the range of steps involved in mRNA localization, including production and transport between and within cells until the final destination in the oocyte. Using Bayesian inference, we calibrate this model using quantitative single molecule fluorescence in situ hybridization data. By analyzing both the steady state and dynamic behaviours of the model, we provide estimates for the rates of different steps of the localization process, as well as the extent of directional bias in transport through the ring canals. The model predicts that mRNA synthesis and transport must be tightly balanced to maintain robustness, a prediction which we tested experimentally using an over-expression mutant. Surprisingly, the over-expression mutant fails to display the anticipated degree of overaccumulation of mRNA in the oocyte predicted by the model. Through careful model-based analysis of quantitative data from the over-expression mutant we show evidence of saturation of transport of mRNA through ring canals. We conclude that this saturation engenders robustness of the localization process, in the face of significant variation in the levels of mRNA synthesis. Statement of significanceFor development to function correctly and reliably across a population, gene expression must be controlled robustly in a repeatable manner. How this robustness is achieved is not well understood. We use modelling to better study the localization of polarity determining transcripts (RNA) in fruit fly development. By calibrating our model with quantitative imaging data we are able to make experimentally testable predictions, comparison of which with data from a genetic mutant, reveals evidence that saturation of RNA transport contributes to the robustness of RNA localization.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Harrison, J. U., Parton, R. M., Davis, I., Baker, R. E.. 2019-02-01. Testing models of mRNA localization reveals robustness regulated by reducing transport between cells. https://doi.org/10.1101/533133

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Dynamic mechanical sorting biases niche occupancy and lineage outcome during development of bilayered glandular epithelia

Tissue compartmentalization into basal and luminal domains is a hallmark of glandular epithelia, yet how fate boundaries are established and stabilized during dynamic morphogenesis remains a major unresolved question. Here, using mouse embryonic explants, organoids, quantitative live imaging and genetic perturbations, we show that basal-luminal compartmentalization is not maintained by fixed boundaries, but through continuous positional corrections. We show that differences in cellular adhesion and actomyosin contractility drive these positional corrections by promoting active cell sorting. We further find that these mechanical differences influence lineage specification by controlling cell positioning rather than directly instructing cell fate. Before commitment, mosaic, but not uniform, perturbation of cell mechanics alters niche occupancy and biases lineage outcome, indicating that relative mechanical properties determine access to fate-instructive niches. Conversely, perturbation of Notch and YAP remodels compartment-specific mechanical properties and cell-positioning dynamics, revealing a reciprocal coupling between lineage state and mechanical sorting. Conservation of this mechanism across four glandular epithelia of distinct origins and functions identifies dynamic mechanical sorting as a general strategy for maintaining robust tissue compartmentalization during the extensive growth and cellular rearrangements of branching morphogenesis.

developmental biology↗

Unbiased lineage tracing across the adipose organ decouples developmental origin from anatomical and transcriptomic identities

The developmental origins of individual adipose depots and whether embryonic lineage dictates adult function remain unresolved. Here, we apply in utero CRISPR-mediated barcoding lineage tracing to construct the first unbiased clonal map of adipose organ development in mice. The developmental hierarchy we uncover challenges several conventions. Remarkably, interscapular brown fat, used as the prototypical brown fat, is the most developmentally isolated brown fat; depots sharing Myf5/Pax3 lineage markers fail to cluster together; mesenteric white fat shares unexpected high clonal ancestry with brown fats despite a radically divergent transcriptome; and subcutaneous white adipose tissues converge transcriptomically despite distant developmental origins. These findings call for a reinterpretation of single-marker lineage tracing data across the adipose organ and propose that adipose depot identity is not solely encoded by embryonic lineage but is substantially shaped by the anatomical niche.

developmental biology↗

Age-dependent mechanical stress underlies unexpected vestibular differentiation and regeneration patterns

Loss of inner-ear sensory hair cells (HCs) is a major cause of hearing and balance disorders. Promoting HC regeneration offers a potential therapeutic strategy, but regenerative capacity is limited in adult mammals and declines rapidly during early postnatal development in mice. HCs can regenerate through trans-differentiation of neighboring supporting cells in a process controlled by Notch mediated lateral inhibition. However, the factors underlying the decrease in regeneration capacity are poorly understood. Here, we combine live imaging with single-HC ablation in mouse vestibular explants to track the dynamics of HC development and regeneration. We reveal unexpected age-dependent deviations from the classical lateral inhibition model, in which new HCs differentiate adjacent to existing HCs. We find that mechanical stress changes with age and that perturbing it alters the observed differentiation patterns. A mathematical model incorporating local mechanical regulation of Notch signaling captures both HC differentiation and regeneration patterns across ages. Together, these findings identify mechanical stress as a crucial regulator of HC differentiation and support an underlying mechanism in which the interplay between local mechanics and Notch signaling shapes regenerative responses. This coupling offers a framework for understanding the age-dependent decline in HC regeneration and motivates investigation of mechanical regulation as a potential therapeutic target.

developmental biology↗