The cooperative antiviral activity of two distinct AGO proteins could be exploited to provide a new strategy for controlling viral diseases in rice.

Mice with a mutation that disrupts the release of growth hormone show greatly increased lifespan, which can be further increased by caloric restriction.

Bacteria use the transcription factor binding region of their transcription activator-like effectors to hijack host basal transcription factor to cause rice diseases by activating host susceptibility genes.

The dramatic extension of lifespan in Sirt6-deficient mice by Trp53 haploinsufficiency suggests that SIRT6 has distinct biological function from SIRT1 in regulating p53 activity and preventing cells from senescence/apoptosis.

The use of tissue culture reduces the chemical modification of plant DNA, and this has lasting effects on gene expression in the plants and their descendants.

The expression of small RNAs (or sRNAs) is regulated not only by mRNA expression, but also by their own regulatory elements and by sRNA biogenesis genes.

Structure-led protein engineering can expand the effector recognition profile of plant intracellular NLR immune receptors, providing a proof-of-principle for the development of novel disease resistance mechanisms in plants.

A new perception of the organization of T-cell receptor repertoires in mice and humans, based on high-throughput sequencing and CDR3 sequence similarity, indicates hubs of cross-species public sequences forming evolutionary conserved 'foci of attention' of T cell immunity.

Tracking individual mice within a group makes it possible to quantify and model social behavior, and reveals that the behavior of the group goes beyond pairwise interactions, and is shaped by complex interactions between multiple individuals.

Transgenic mice with Rett-causing mutations in MeCP2 reveal that a basic cluster in the C-terminus of the protein binds DNA and that both the methyl-CpG binding domain and the transcriptional repression domain are necessary to elicit toxicity in MECP2 duplication syndrome.