Search bioRxiv⌕ Search

bioRxiv · 10.1101/677641

An in silico analysis of robust but fragile gene regulation links enhancer length to robustness

Abstract

1Organisms must ensure that expression of genes is directed to the appropriate tissues at the correct times, while simultaneously ensuring that these gene regulatory systems are robust to perturbation. This idea is captured by a mathematical concept called r-robustness, which says that a system is robust to a perturbation in up to r - 1 randomly chosen parameters. In this work we use this idea to investigate the robustness of gene regulation using a sequence level model of the Drosophila melanogaster gene even-skipped. We find that gene regulation can be remarkably sensitive to changes in transcription factor concentrations at the boundaries of expression features, while it is robust to perturbation elsewhere. We also find that the length of sequence used to control an expression feature correlates negatively with the number of nucleotides that are sensitive to mutation in both natural and in silico predicted enhancers. In all cases, the exact degree of robustness obtained is dependent not only on DNA sequence, but also on the local concentration of regulatory factors. By analyzing both natural and synthetic sequences, we provide strong quantitative evidence that increased sequence length makes gene regulatory systems more robust to genetic perturbation.\n\n2 Author SummaryRobustness assures that organisms can survive when faced with unpredictable environments or genetic mutations. In this work, we characterize the robustness of gene regulation using an experimentally validated model of the regulation of the Drosophila gene even-skipped. We use a mathematically precise definition of robustness that allows us to make quantitative comparisons of robustness between different genetic sequences or between different nuclei. From this analysis, we found that genetic sequences that were not previously known to be important for gene regulation reduce sensitivity to genetic perturbation. In contrast, we found that gene regulation can be very sensitive to the levels of regulators. This extreme sensitivity was only observed at the boundaries of expression features, where switch-like behavior is desirable. This highlights the importance of considering context when assessing robustness.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Barr, K. A., Reinitz, J., Radulescu, O.. 2019-06-21. An in silico analysis of robust but fragile gene regulation links enhancer length to robustness. https://doi.org/10.1101/677641

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

KEEP EXPLORING

Related preprints

Three-dimensional mapping of human lung fibrosis identifies spatial coupling between tissue microarchitecture and maladaptive repair states

Human lung fibrosis progressively destroys three-dimensional tissue architecture, yet how the structural microenvironment shapes cellular states remains unclear. Integrating 3D X-ray histology with spatial omics, we generate a volumetric multimodal atlas of human lung fibrosis that enables direct interrogation of relationships between tissue microarchitecture and spatial molecular programmes. We identify collapse of the alveolar-capillary unit - the coupled loss of alveolar type 1 epithelial cells, capillary endothelial cells, and basement membrane integrity - as a structural transition associated with early fibrogenesis. Surrounding transitional zones exhibit aberrant epithelial differentiation and proteolytic matrix remodelling, with epithelium shifting toward bronchiolised, airway-like states. Stromal activation converges on spatially restricted fibrogenic cores, sites of maximal collagen maturation and matrix stabilisation that function as signalling hubs within surrounding perifocal and vascular microenvironments. Molecular signatures of atlas-defined tissue states were associated with lung function and mortality across independent patient cohorts. Together, these data support a model in which fibrosis emerges as a spatial tissue-state process, with alveolar-capillary collapse redirecting repair towards mechanically stabilised niches that reinforce pathological remodelling.

systems biology↗

A three-factor model can explain symmetry breaking and the n-1 rule during X-chromosome inactivation

X-chromosome inactivation (XCI) is a mammalian gene regulatory process that via chromosome-scale transcriptional silencing, leaves active a single X chromosome per diploid genome complement. The mechanisms that enable cells to select the appropriate number of X chromosomes to inactivate while leaving others active remain unclear. We demonstrate that all known chromosomal counting scenarios during XCI can be accounted for by a three-factor mathematical model that includes (1) Xist, the long noncoding RNA (lncRNA) responsible for gene silencing during XCI in eutherians, (2) an X-linked transcriptional activator of Xist, and (3) the autosomally-encoded SPEN, an Xist RNA-binding protein that is essential for gene silencing during XCI. In our model, symmetry between active X chromosomes is broken by stochastic differences in the number of Xist molecules that associate with the X chromosomes at the onset of XCI. Subsequently, integrated positive and negative feedback loops amplify then propagate superstoichiometric assemblies of SPEN complexed with Xist on the inactive chromosome(s), and select for levels of X-linked activator that enable only one X chromosome per diploid genome complement to remain active. Thus, asymmetric propagation of the SPEN-Xist ribonucleoprotein complex may play an essential role in symmetry breaking and chromosomal counting during XCI, independently of or in concert with cis-acting networks of DNA regulatory elements. Our results also have conceptual implications for gene regulatory circuits on autosomes.

systems biology↗

stem.MAP: Identification of cell-type-specific protein complexes in mammalian embryonic stem cells.

Protein complexes carry out critical functions during development. Mapping cell-type-specific protein complexes in early embryogenesis is essential for uncovering the molecular mechanisms of embryonic development. We unfortunately currently lack a catalog of protein complexes specific for embryogenesis including embryonic stem cells. Here we develop a proteomics-based machine learning workflow to predict protein complexes present in mouse embryonic stem cells (mESC). Our method integrates data from a cell-type agnostic protein complex resource with co-fractionation mass spectrometry (CF-MS) experiments on mESC. Our resource, stem.MAP, identifies 3,986 complexes encompassing ~133,000 unique interactions, and 8,616 proteins. stem.MAP captures variant complexes critical for stem cell function including the PRC2, BAF and NuRD complexes. stem.MAP also discriminates mutually exclusive interactions specific to embryonic stem cells (e.g. Eif4ebp2 - Eif4e). Finally we observe 1,388 high confidence stem.MAP interactions found only in mESC CF-MS data, many with support from AlphaFold modeling and a gastruloid coregulation network. We make stem.MAP protein complexes available through our web resource: stem.proteincomplexes.org. We anticipate stem.MAP will be beneficial to the study of early development and we expect our proteomics-based machine learning workflow to be applicable to the creation of any context-specific protein interaction network.

systems biology↗