Harmful genetic variants at mendelian disease genes slow down adaptation, by interfering with the spread of adaptive variants in a population.

Lesions to the anterior-medio-dorsal thalamus cause widespread behavioral impairments across multiple cognitive domains, suggesting that thalamic hubs are critical for interconnecting diverse cognitive processes.

Postnatal, postsynaptic loss of FMRP specifically weakens callosal synaptic inputs onto L2/3 pyramidal neurons, in requirement ofnormal sensory experience, through downregulating AMPA receptor transmission and without affecting local synaptic inputs during cortical circuit development.

Senescent cells accumulate in the fracture callus and a reduction in the number of these cells accelerates fracture healing in mice.

The nutrient composition of food alters both the size of gut epithelial cells and the ability of the stem cell niche to control tissue turnover, resulting in changes in size at the organ level.

Aging is associated with stress-induced senescence of adipose stromal cells, leading to impaired adipogenesis, oxidative stress, mitochondrial dysfunction, and insulin resistance, all being alleviated by metformin treatment of adipose stromal cells.

Multidimensional analysis of data from high-throughput behavioral assays reveals many independent axes of behavioral variation among inbred animals reared in the same environment.

Quantitative FRET imaging in moving C. elegans shows that stretch-unfolding of twitchin kinase occurs in the active muscle, whereby mechanical activity titrates the signaling pathway of this cytoskeletal kinase.

Topoisomerase IV and the ter-binding protein MatP competitively bind the hinge domain of the Escherichia coli Structural Maintenance of Chromosomes complex, MukB, leading to spatiotemporal regulation of MukBEF-topoisomerase IV activity.