When exposed to high-dose ionizing radiation, tardigrades undergo extensive DNA damage, like humans, but cope by stimulating expression of DNA repair proteins and of TDR1, a novel tardigrade-specific DNA-binding protein.

Hybridization not only generates genetic diversity, but this diversity can alter the shape of the fitness landscape, changing which genotypic combinations are favored by natural selection and which accessible genotypic paths lead to novel fitness peaks.

Experiments on E. coli show that multiple mechanisms contribute to extreme resistance to ionizing radiation in bacteria, with mutations to three genes for DNA repair having a prominent role in one evolved population.

The optimal allocation strategy prioritizes funding to high-transmission settings in sub-Saharan Africa, but highlights a trade-off between reducing clinical malaria burden and reducing the global population at risk of malaria.

Machine learning and experimental tests of receiver bias identify signal components critical to correct species classification in guenons, linking face pattern diversity to selection for species discrimination.

CPT1A downregulation enhances radioresistance in colorectal cancer (CRC) via FOXM1-mediated antioxidant response, making it a potential biomarker for radiosensitivity and a novel target for improving CRC radiotherapy.

The evolution columbine genus involved frequent mixing between incipient species, and one chromosome appears to have taken its own path.

Tiny animals known as tardigrades use a combination of DNA repair machinery and a novel protein to mend their genome after intense ionizing radiation.

Late effects of radiation therapy in mice can be prevented by treatment with either senolytics navitoclax or quercetin plus dasatinib or the senostatic metformin.

A three-dimensional investigation of extinct-tetrapod limbs shows that even though bone elongation and blood-cell production are intimately related to mammal long bones, these functions actually appeared successively in tetrapod evolution.