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Tica, J.

Publications and source records attributed to Tica, J..

2 recordsLinked to original sources

A three-node Turing gene circuit forms periodic spatial patterns in bacteria

Turing patterns1 are well-known self-organising systems that can form spots, stripes, or labyrinths. They represent a major theory of patterning in tissue organisation, due to their remarkable similarity to some natural patterns, such as skin pigmentation in zebrafish2, digit spacing3,4, and many others. The involvement of Turing patterns in biology has been debated because of their stringent fine-tuning requirements, where patterns only occur within a small subset of parameters5,6. This has complicated the engineering of a synthetic gene circuit for Turing patterns from first principles, even though natural genetic Turing networks have been successfully identified4,7. Here, we engineered a synthetic genetic reaction-diffusion system where three nodes interact according to a non-classical Turing network with improved parametric robustness6. The system was optimised in E. coli and reproducibly generated stationary, periodic, concentric stripe patterns in growing colonies. The patterns were successfully reproduced with a partial differential equation model, in a parameter regime obtained by fitting to experimental data. Our synthetic Turing system can contribute to novel nanotechnologies, such as patterned biomaterial deposition8,9, and provide insights into developmental patterning programs10.

synthetic biology↗

Rats and axolotls share a common molecular signature after spinal cord injury enriched in collagen-1

Spinal cord injury (SCI) in mammals leads to irreversible tissue damage and loss of function. In contrast, axolotls are able to regenerate scar-free the injured spinal cord. To explore new pathological mechanisms, we compared rat versus axolotl transcriptomics and isolated genes shared between species post-SCI. Unexpectedly, multiple transcripts involved in extracellular matrix remodelling, in particular collagen-1, were upregulated in both species after SCI. Proteomics validated persistent expression of the collagen-enriched matrix signature at the protein level. Collagen-1 accumulated in early and advanced rat lesions. Importantly, collagen-1 was likely associated with pathological vascular remodelling rather than classic fibrosis and the transcription factor SP1 was predicted and validated to regulate, at least in part, the expression of collagen-1 in rat lesions.

pathology↗