Substantial heritable genetic variation in adaptability and the pleiotropic consequences of adaptation exists in budding yeast, and can be explained by a combination of fitness and specific segregating alleles.
Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.
Cryo-EM structures reveal how the peptidisc scaffold can adapt to different membrane proteins, establishing it as a universal membrane mimetic to stabilize membrane proteins in solution.
An experimentally constrained model shows that Escherichia coli faces fitness trade-offs in chemotaxis behaviors, and that adaptation of phenotypic diversity through altered gene regulation permits populations to resolve these trade-offs.
A distinctive novel mechanism of ephrin-A/EphA signaling modulation in retinal growth cones ensures concurrent quantitative accuracy and adaptability of topographic hardwiring.
Experimentally evolved yeast populations increase in fitness predictably but do not divide into coexisting lineages or dramatically increase their mutation rates after 10,000 generations.
Fluctuation of biomarkers is a novel way of studying system stability during stable and unstable states of health and disease, revealing the systems' ability to cope with external perturbations.
Selective forces imposed by the squid animal host drive rapid adaptation of non-native Vibrio fischeri bacteria through convergent mutations of large effect, unmasking preexisting coordinated regulation of symbiosis.
The immune effector Drosomycin buffers stress signaling in hypertrophic salivary glands to inhibit their disintegration, detection by the cellular immune response, and promotes further overgrowth.
