Interbreeding between Neanderthals and modern humans was strongly sex biased

When Neanderthals and anatomically modern humans (AMHs) interbred, the encounters were not random between the sexes. Researchers examined the relative proportions of Neanderthal and AMH ancestry on X chromosomes versus autosomes in both populations. They found a 62% relative excess of AMH ancestry on Neanderthal X chromosomes, which allowed them to characterize the direction of gene flow: pairings predominantly involved male Neanderthals and female AMHs. Using analytical and numerical modeling, they compared two possible explanations—differential male and female migration patterns versus mate preference—and found mate preference to be the simpler, more likely driver of this sex bias. The findings add to growing evidence that sex-biased demographic processes were a recurring feature of human evolutionary history, and they refine our understanding of how and under what social or behavioral circumstances these two hominin groups mixed.

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A cellular basis for the mammalian nocturnal-diurnal switch

Researchers investigated why some mammals are active during the day while others are nocturnal, focusing on the cellular machinery that might underpin this behavioral divide. Using comparative cell biology and genomics across diurnal and nocturnal species, they discovered that cells from daytime-active mammals maintain more stable protein synthesis, phosphorylation, and circadian clock function across varying temperatures compared to cells from night-active species. Genomic analysis pointed to accelerated evolutionary changes in signaling pathways, particularly mTOR, that make diurnal circadian clocks more resistant to thermal and osmotic stress. Crucially, when mTOR was pharmacologically inhibited in nocturnal mice, their cells, tissues, and behavior shifted toward daytime activity patterns. The findings suggest that after the extinction of dinosaurs opened daytime ecological niches, changes in intracellular signaling networks—rather than just neural or hormonal factors—provided the molecular foundation for mammals to transition from nocturnal to diurnal lifestyles.

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Imbalance in gut microbial interactions as a marker of health and disease

Researchers developed a new way to characterize gut microbiome imbalance by focusing on the ecological relationships between microbes rather than just their abundance. They built a mathematical model of gut microbiome dynamics that revealed two alternative stable states: a healthy community dominated by competitive (negative) microbial interactions, and a dysbiotic community dominated by cooperative (positive) ones. Inspired by this finding, they created the Ecological Network Balance Index (ENBI), which quantifies the ratio of positive to negative microbial interactions within a community. Testing ENBI across simulated and real patient datasets covering multiple diseases, they found it reliably distinguished healthy from dysbiotic states and tracked disease progression in conditions like colorectal cancer. Because existing dysbiosis markers largely ignore ecological mechanisms, ENBI offers a more biologically grounded diagnostic signal and could potentially help identify disease onset or severity through microbiome interaction patterns.

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Different DNA repair pathways support intact or truncated insertions by R2 retrotransposon protein

Researchers investigated how the R2 retrotransposon protein, which copies RNA into DNA and inserts it at specific genomic sites, completes stable integration — a poorly understood step in the process called target-primed reverse transcription. Using a screen for cellular factors affecting site-specific transgene insertion into the human genome, they found that three distinct DNA repair pathways compete to resolve the intermediate structure created after reverse transcription. Depending on which pathway acts — ATR-dependent polymerase θ end joining, 53BP1/shieldin/CST–polymerase α–primase fill-in synthesis, or CtIP-MRN-dependent strand annealing — the resulting insertions differ in length and in the DNA sequence signatures at their junctions. This means insertion outcome is shaped by the cell's own repair machinery rather than being dictated solely by the retrotransposon protein itself. The findings clarify the final steps of non-LTR retrotransposon integration and have implications for understanding natural transposon mobility and for improving genome engineering tools.

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Convergent and lineage-specific genomic changes shape adaptations in sugar-consuming birds

Multiple bird lineages — hummingbirds, parrots, honeyeaters, and sunbirds — independently evolved the ability to thrive on diets rich in sugar that would cause metabolic disease in humans. To understand how, researchers sequenced nine new bird genomes and generated 90 tissue-specific transcriptomes across these groups. Comparative genomic analysis uncovered repeated selection at both protein-coding and regulatory regions, pointing to shared genetic solutions arising independently in different lineages. Affected genes are linked to blood pressure, lipid handling, amino acid processing, and carbohydrate metabolism. Functional experiments confirmed altered activity in honeyeater hexokinase 3, an enzyme central to glucose processing. Notably, MLXIPL — a master regulator of sugar and lipid balance — showed convergent sequence and expression changes across all sugar-feeding groups, and hummingbird MLXIPL demonstrated heightened transcriptional responses to sugar. The findings reveal both shared and lineage-specific genomic strategies underlying repeated adaptation to high-sugar feeding in birds.

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Organism-wide cellular dynamics and epigenomic remodeling in mammalian aging

Researchers built a large-scale single-cell atlas of chromatin accessibility—a measure of how open and active different genomic regions are—across 21 tissues in mice at three ages and in both sexes. Roughly a quarter of the hundreds of cell types identified showed meaningful changes in their relative abundance with age. Cells from related lineages distributed across multiple organs shifted in coordinated ways, pointing to systemic signals rather than purely local effects. The team pinpointed both internal molecular drivers, such as shifts in transcription factor activity, and external ones, including cytokine signaling programs, as contributors to these age-related changes. Notably, about 40% of aging-associated shifts in cell populations differed between males and females, with tens of thousands of genomic sites changing in a sex-specific manner. The work provides a detailed, organism-wide picture of how aging restructures both tissue composition and gene-regulatory landscapes.

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