Proper development depends on establishing precise gene expression patterns in spite of the inherent noise in transcription, shadow enhancers buffer this noise by binding distinct input transcription factors.
Tracheal and esophageal fate specification underlies human structural anomalies, multiple cancers, and human pluripotent stem cell approaches for generating respiratory and esophageal cell types for tissue engineering.
Human learning relies on short-term memories (eligibility traces) which provide a mechanism to reinforce sequences of actions from a single reward (one-shot).
There is a strand-based evolutionary mechanism for the diversification of outer membrane proteins, which has implications for how repeat proteins are created and for how outer membrane proteins fold.
The Drosophila tracheal fate is stabilized by the combination of transcriptional programs to control tissue architecture and tissue-level input sensitive to tubular geometry, ensuring the robust mechanism of organ determination.
Cells in the tracheal systems of fruit fly larvae are organised into compartments with precisely located boundaries, which pattern the formation of branched tubular networks.
Tracheal-derived matrix metalloproteinase 1 activity sustains tracheal branch invasion into myotubes by modulating ECM properties and dynamic behavior of sprouting tip cells.
Cell-cell junctions and the actin cytoskeleton are key players in the organisation and patterning of the extracellular matrix (ECM) on the apical side of tracheal cells.
Astrocyte microdomain calcium transients are mediated by TrpML, stimulated by ROS and tyramine, and mediate astrocyte–tracheal interactions in CNS gas exchange.
