The yeast mRNA decapping enzyme Dcp1/Dcp2 repressses many genes whose products are required on poor carbon or nitrogen sources in nutrient-replete cells by mRNA decapping and degradation or translational repression, adding post-transcriptional controls to the transcriptional repression of these functions.

Imaging of neurons within the hippocampus, a memory region of the brain, reveals how the brain updates memories during different learning conditions compared to when learning is blocked by amnestic drugs.

To see the world stable across saccades, the brain compensates retinal shifts induced by the movements, pre-saccadic maps of sensitivity reveal that this process takes time and follows attentional dynamics.

Both hand and face representations remain relatively stable after arm amputation in adulthood, with no link to phantom limb pain, whereas pre-natal limb loss triggers complex patterns of remapping that do not relate to cortical topography.

Dhh1, Pat1, and Lsm1 target subsets of cellular mRNAs for decapping via interactions of these regulatory proteins with the C-terminal domain of Dcp2, the catalytic component of the decapping enzyme.

For mRNA decapping by enhancing DCP2's mRNA-binding affinity and regulating distinct biological processes through DCP1a and DCP1b, human DCP1 is essential.

The effect of genetic variation on gene expression can be specific down to the level of individual cells.

A functional connectivity gradient in striatum is obtained that maps onto DaT SPECT-derived dopaminergic projections and thereby likely provides a new biomarker for investigating dopaminergic (dys)function in the human brain.

A bulk barcoded quantitative trait locus approach increases the power and resolution of genotype-phenotype mapping in yeast, revealing that the genetic architecture of 18 complex traits is highly polygenic, and is characterized by widespread epistatic interactions and pleiotropic effects.

Genome-wide mapping of heteroduplex DNA (a recombination intermediate) formed during mitotic recombination in yeast demonstrates that the "classical" model of double-strand DNA break repair is inadequate to explain several aspects of mitotic recombination.