Current Biology最新文献

Frugivore preferences for rare fruits are a powerful mechanism for plant diversity maintenance. Nevertheless, the drivers of frugivore preferences and avoidances remain unknown. Using 12 years of bimonthly data on plant-frugivore interactions and fruit counts collected in Portugal, we assessed the contribution of fruit nutritional and energetic composition and heterospecific density-dependent effects to frugivore preferences and avoidances. We found that preferences were higher and avoidances lower for rare fruits with more distinctive fruit compositions. Moreover, we detected negative effects of neighboring fruit density on frugivore avoidances, but not on preferences, suggesting that neighboring plants facilitate interactions of the surrounding plant community by attracting birds to the area. Our results provide the first empirical evidence of the diet-complementarity hypothesis as a driver of rare-biased seed dispersal, likely contributing to global plant biodiversity maintenance.

The typical ant colony consists of reproductive females ('queens'), non-reproductive females ('workers') and males that die shortly after mating¹. Rare deviations from this standard pattern² include the loss of workers in socially parasitic ants³ ('inquilines') and the absence of males in a few parthenogenetic taxa⁴. Here, we add a new variant: Temnothorax kinomurai⁵ is the first ant species known to lack both workers and males and to consist exclusively of queens.

Alexander Gann details the life and work of the molecular biologist, author, and administrator James Watson, who co-discovered the double helical structure of DNA.

A new study shows that invasive American bullfrogs restructure island food webs by displacing native species from central roles, increasing network connectance and reducing modularity. These changes destabilize ecosystems and decouple food-web architecture from classic island biogeography patterns, revealing hidden invader impacts beyond species loss.

Molecular motor proteins are important mechanical regulators of many cellular processes, yet measuring their force production in cells has been a challenge. A new paper describes the first FRET-based sensor to measure motor forces during meiotic cell division.

Neurons continuously adjust their properties as a function of experience. Precise modulation of neuronal responses is achieved by multiple cellular mechanisms that operate over a range of timescales. Primary sensory neurons not only rapidly adapt their sensitivities via posttranslational mechanisms, including regulated trafficking of sensory molecules,^1,2,3,4 but also alter their transcriptional profiles on longer timescales to adapt to persistent sensory stimuli.^5,6,7,8 How diverse transcriptional and posttranscriptional pathways are coordinated in individual sensory neurons to accurately adjust their functions and drive behavioral plasticity is unclear. Here, we show that temperature experience modulates both transcription and trafficking of thermoreceptors on different timescales in the C. elegans AFD thermosensory neurons to regulate response plasticity. Expression of the PY motif-containing adaptor protein (PY motif transmembrane 1 [PYT-1]), as well as the GCY-18 warm temperature-responsive guanylyl cyclase thermoreceptor,⁹ is transcriptionally upregulated in AFD upon a temperature upshift.^5,10 We find that as GCY-18 begins to accumulate at the AFD sensory endings, the GCY-23 cooler temperature-responsive thermoreceptor⁹ exhibits altered subcellular localization and increased retrograde trafficking, thereby increasing the functional GCY-18 to GCY-23 ratio in the AFD sensory compartment. Altered GCY-23 localization and trafficking require PYT-1-dependent endocytosis, and we show that PYT-1-mediated modulation of the GCY-18 to GCY-23 protein ratio at the AFD sensory endings is necessary to shift the AFD response threshold toward warmer values following the temperature upshift. Our results describe a mechanism by which transcriptional and posttranscriptional mechanisms are temporally coordinated across sensory receptors to fine-tune experience-dependent plasticity in the response of a single sensory neuron type.

Archaea of the order Sulfolobales possess a eukaryote-like cell division machinery and display a eukaryote-like cell cycle; however, the cell division and cell-cycle control mechanisms remain enigmatic. Here, we demonstrate that phosphorylation of the α subunit by a eukaryote-like protein kinase, ePK2, affects 20S proteasome assembly and controls cell division in Saccharolobus islandicus. ePK2 exhibits cell-cycle-dependent expression at both transcriptional and translational levels. Deletion or overexpression of epk2 results in impaired cytokinesis, with the deletion cells being unable to generate single chromosome cells after synchronization and the overexpression cells exhibiting growth retardation and cell enlargement. Interestingly, overexpression of ePK2 leads to a coherent reduction in cellular proteasome activity and degradation of cell division proteins. We identify S200 and T213 of the proteasome α subunit as specific target sites for ePK2 phosphorylation. Functional analyses of site-directed mutants at S200 and T213 suggest that phosphorylation at these two residues disrupts the assembly of de novo 20S proteasome. Collectively, our study uncovers an ingenious and efficient mechanism of proteasome phosphorylation-mediated cell division regulation, a prototype of the eukaryotic cell-cycle regulation system, in Sulfolobales archaea.

Assigning valence-appeal or aversion-to gustatory stimuli and relaying it to higher-order brain regions to guide flexible behaviors is crucial to survival. Yet the neural circuits that transform taste into motivationally relevant signals remain poorly defined in any model system. In Drosophila melanogaster, substantial progress has been made in mapping the sensorimotor pathways encoding intrinsic valence for feeding and the architecture of the dopaminergic reinforcement system. However, where and how "effective" (i.e., real-time) valence is first imposed on a taste has long been a mystery. Here, we identified a pair of subesophageal zone interneurons in Drosophila, termed Fox, that impart reinforcing positive valence to sweet taste and convey this signal to the mushroom body, the fly's associative learning center. We show that Fox neuron activity is necessary and sufficient to drive appetitive behaviors and can override a tastant's intrinsic neutral or aversive valence without impairing taste quality discrimination. Furthermore, Fox neurons relay the positive valence to specific dopaminergic neurons that mediate appetitive memory formation. Our findings reveal a circuit mechanism through which effective valence is bestowed upon sweet sensation and transformed into a reinforcing signal that supports learned sugar responses. The Fox neurons form a convergent-divergent "hourglass" circuit motif, acting as a bottleneck for valence assignment and distributing motivational signals to higher-order centers. This architecture confers both robustness and flexibility in reward processing-an organizational principle that may generalize across species.

Mitochondria contain a genome (mtDNA) encoding a handful of proteins essential for cellular respiration. mtDNA can leak into the cytosol and drive fitness defects. The first genes associated with mtDNA escape were discovered in yeast and aptly named "yeast mitochondrial escape" (YME) genes. We identify the mechanism by which an intermembrane space nuclease, endonuclease G (human ENDOG; yeast Nuc1), prevents mtDNA escape to the cytosol in yeast. Nuc1 nuclease activity and mitochondrial localization are essential for preventing mtDNA escape and suggest a direct role of Nuc1 in degrading mtDNA bound for escape. We find that blocking autophagy via atg1 and atg8 mutants prevents mtDNA escape in the absence of Nuc1. We further demonstrate that blocking mitophagy via atg11 and atg32 mutants prevents mtDNA escape, whereas inducing mitophagy increases mtDNA escape in the absence of Nuc1. Finally, we demonstrate that Nuc1 degrades mtDNA bound for escape via the vacuole, as an atg15 mutant that prevents disassembly of autophagic bodies in the vacuole also prevents mtDNA escape. Overall, our results implicate vacuolar entry of mitochondria during mitophagy as an important mtDNA escape pathway in yeast, which is normally mitigated via the degradation of mtDNA by Nuc1.