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Biology subjects

Tambo, M.

Publications and source records attributed to Tambo, M..

2 recordsLinked to original sources

Coupling Mechanical Regulation with Biochemical Reaction-Diffusion Circuits Yields Robust Self-Organized Pattern Formation.

Cell-cell signaling circuits that combine local self-activation with long-range inhibition have long been proposed as a theoretical mechanism sufficient to generate cellular patterns, such as spots and stripes. Here we construct synthetic pattern-forming circuits, implementing local self-activation (positive feedback) using juxtacrine synNotch receptor interactions, and implementing long-range inhibition using diffusible competitor molecules. While combining local positive feedback with long-range inhibition leads to more spatially heterogeneous cell states, these synthetic circuits do not robustly lead to well defined patterns. We find, however, that if we couple these reaction-diffusion circuits with induction of genes that regulate cell mechanics - such Cadherin molecules that promote local cell adhesion and sorting - we observed the emergence of much more well-defined cellular patterns. Theoretical analysis indicates while reaction-diffusion circuits can be sufficient to generate patterns under precisely balanced parameter conditions, the close coupling of cell mechanical/sorting significantly increases the robustness of pattern formation (the parameter space yielding patterns). Thus, circuits that closely integrate signaling and mechanical changes may underlie many evolved morphogenic pattern formation systems.

synthetic biology↗

Detailed single-cell mapping of the transcriptional response to a virus infection driven by copy-back viral genomes

The antiviral response to several clinically significant viruses, including respiratory syncytial virus and parainfluenza virus, is driven by copy-back viral genomes (cbVGs) generated during virus replication. However, the broader impact of cbVGs on the functional states of host cells remains undefined. Here, we developed a single-cell RNA-sequencing and computational framework to map cbVG-driven host responses during Sendai virus infection. Unsupervised profiling identified distinct transcriptional states throughout the course of infection, highlighting a shift from early antiviral signaling to later inflammatory and remodeling programs. Stratifying infected cells by cbVG status demonstrated that cbVG-positive cells initiate interferon and chemokine programs, which later spread to cbVG-negative cells. At later stages, cbVG-positive cells acquire additional signaling, cytoskeletal, transcriptional, and stress-adaptation programs, which are absent in cbVG-clean infection. This work defines the broader cbVG-driven layered and dynamic host response and provides a valuable high-resolution resource of the temporal cellular response to a virus infection.

microbiology↗