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.

The probability of a cellular response to a differentiation inducing signal is correlated with the dynamic expression of a Ras protein, and produces a ‘salt and pepper’ pattern of cell differentiation.

The convergent evolution of unusually strict substrate specificity in apicomplexan LDHs arose by classic neofunctionalization of a duplicated MDH gene via few mutations of large effect.

The development of the electrical phenotype of neurons can be precisely quantified and dissected using a combination of multi-variate statistical analyses and a systematic electrophysiological characterization of electrical properties.

The kinesin-14 motor Kar3 moves along microtubules using a previously undescribed mechanism that critically requires the presence of a non-catalytic head.

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

Interviews with senior biomedical researchers reveal a perceived decline in trust in the scientific enterprise, in large part because the quantity of new data exceeds the field's ability to process it appropriately.

A new dynamic mechanistic model explains how the destruction complex negatively regulates Wnt signaling in development and oncogenesis.

Enzyme evolution is reversible on a structural and functional (phenotypic) level, but through a different mutational pathway that leads to genotypic incompatibility with the ancestor.

A long-term evolution experiment with Escherichia coli shows that the appearance and optimization of a new trait can require both co-opting existing cellular pathways for new roles and reversing a history of previous adaptation.