Evolutionary novelty is promoted by a macroevolutionary pulse of developmental plasticity, but is enhanced by secondary fixation, which permits developmental character release and further morphological exploration.
Analysis of neurons that lack the two neuronal dynamins, dynamin 1 and 3, demonstrates a pathway of synaptic vesicle reformation that does not require these two dynamins or clathrin-dependent budding.
Epsin has a key role in the coupling of actin to endocytic clathrin coated pits that is required for their maturation and helps capture SNAREs at endocytic clathrin coated pits.
Using iPSCs as a model to study neurodevelopmental differences between human and nonhuman primates lays the groundwork for understanding aspects of human brain evolution and neurological disease susceptibility.
Loss of an amino acid transporter and tissue depletion of nitric oxide worsens the intestinal function of CF mice, a finding that potentially explains variation in disease severity amongst CF individuals.
Cellular carbon accumulation systems are a fundamental prerequisite for biomineralization to stabilize pH and to supply inorganic carbon for CaCO3 precipitation under changing environmental conditions.
The substrate for evolutionary divergence does not lie in changes in neuronal cell number or targeting, but rather in sensory perception and synaptic partner choice within invariant, prepatterned neuronal processes.
Tracheal-derived matrix metalloproteinase 1 activity sustains tracheal branch invasion into myotubes by modulating ECM properties and dynamic behavior of sprouting tip cells.
A novel mutation in SCGN is associated with risk for inflammatory bowel disease and implicates the intestinal neuroendocrine compartment in the pathogenesis of this disorder.
Multi-modal structural data fusion questions the specificity of fMRI-behavior associations by providing strong evidence relating human brain structure to a wide range of behavioral measures previously associated to functional connectivity.
