A combination of neuroscience approaches and indirect calorimetry demonstrate a physiological role for AgRP neurons in cold-induced hyperphagia and strongly suggest temperature is an important regulator of AgRP neuron activity.

A diverse group of modifier genes, including the proto-oncogene Src, cooperate with Notch specifically to control cell proliferation.

Gene regulation by C/EBPβ determines how surplus of dietary fat is stored, which has consequences for metabolic health.

For skeletal muscle in mice, the size of the stem cell pool can be uncoupled from overall tissue size allowing for a dramatic increase in stem cell number.

Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.

Mutations in CHD7, which cause CHARGE syndrome, cause a reduction in FGF8 signalling and subsequent abnormalities in the cerebellar vermis in both mice and humans.

Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.

A mouse mutant in which nearly all dentate gyrus granule cells fail to develop provides a new window on the role of the dentate gyrus in spatial learning and memory.

Depleting Mi-2 in the progeny of neural stem cells prevents normal enhancer decommissioning so that they become sensitive to Notch activity and re-acquire stem cell properties.

Down-regulation of GAS6 by M1 macrophages resulted in impaired efferocytosis for synovial apoptotic cells, causing synovial hyperplasia and obesity-associated OA development.