BMC Biology最新文献

Background: Nutrition during early life often has lasting consequences for adult physiology. However, it remains unclear how developmental diet shapes both the initial energetic state and subsequent change of energy stores. To address this, we systematically varied yeast and sugar concentrations in the developmental diet of Drosophila melanogaster and quantified energy reserves (in joules, derived from fat, glycogen, trehalose, and glucose) at eclosion and after 10 days of adulthood on a standardized diet. Comparing these time points allowed estimation of net change in energy reserves. Additionally, we examined how these effects depend on sex, population, and reproductive status.

Results: Developmental diet strongly influenced initial energy reserves. Higher sugar concentrations increased energy stores at eclosion. However, the subsequent net change in energy was inversely related to these starting conditions. Flies reared on high-sugar larval diets, which emerged with the most energy, exhibited the smallest net change during early adulthood. In contrast, flies from low-sugar diets emerged leaner and subsequently showed the largest net increase. These patterns were modulated by sex and reproductive status. In males, energy stores more closely reflected the larval nutritional background, whereas in females this relationship was weaker-likely due to the energetic demands of oogenesis. Mating was generally associated with lower energy reserves across groups.

Conclusions: Early-life diet affects both the starting point and early-adult change in energy reserves in Drosophila. These findings outline a framework in which developmental history and adult conditions jointly shape energetic trajectories.

Nictation is a dispersal behavior in nematodes, aiding movement and host-finding under stress. This review explores its diversity, genetic and neuronal basis, regulation, and ecological relevance. Nictation involves sensory integration, plasticity, and inter-organismal communication. Though its neural circuitry and molecular pathways remain partly understood, recent findings highlight roles for dauer signaling, neurotransmitters, and neuropeptides. Advances in scoring methods and genetic tools, including of parasitic species, now enable deeper study of its environmental triggers, evolutionary context, and impact on nematode virulence, with key knowledge gaps identified for future research.

Background: The black soldier fly (BSF, Hermetia illucens) is widely used for waste bioconversion and sustainable protein production. However, domestication and prolonged captive rearing can rapidly alter genetic diversity and population structure. This study investigated how selective breeding, genetic drift, and relaxed selection have shaped genomic variation and effective population size in multiple BSF populations. Using genome-wide restriction site-associated DNA sequencing, we analysed population structure, heterozygosity, and selection signatures across 11 BSF populations, including 1 long-term domesticated line, 5 selectively bred lines (Line A to Line E), 3 wild-derived populations, and 2 commercial strains.

Results: Despite shared origins, lines LA to LE diverged rapidly within 6 years. Principal component analysis and ADMIXTURE clustering (K = 11) revealed that LC to LE retained close genetic affinity, while LA and LB diverged markedly from each other and LC-LE. Demographic reconstructions using Stairway Plot showed that effective population sizes increased during the initial homogenized selective breeding phase (2018-2019) but declined after 2022, consistent with bottlenecks and relaxed selection. Wild-derived populations maintained higher heterozygosity and lower inbreeding coefficients than domesticated lines. Finally, genome-wide analyses identified 133 candidate genes under selection, including signatures of balancing selection and selective sweeps, reflecting divergent evolution under domestication.

Conclusions: These findings demonstrate that genetic differentiation occurs rapidly in BSF populations under domestication, driven by artificial selection, relaxation, genetic drift, and environmental adaptation. These results highlight the need for genetic monitoring in breeding programmes, including maintenance of large founder populations, periodic genetic assessment, and genetic rescue to preserve adaptive potential and reduce inbreeding risks.

Background: Anthropogenic forces have resulted in staggering losses of biodiversity and population declines in many species over the past two centuries. Associated with these declines are potential adverse effects linked to small population sizes, including loss of genetic diversity and increased levels of inbreeding. Here, we leverage DNA sequencing from museum specimens to examine genetic variation between historic and contemporary populations of four species of warblers (Aves, Setophaga) that vary with respect to degree of population changes over this period. To explore the genetic impacts of varying population declines, we gathered polymorphism data at 157 PCR-amplified loci in 341 individuals sampled in two time periods-historic (1789-1955) vs contemporary (2001-2020).

Results: For all four species, we observed decreases in nucleotide diversity and heterozygosity in contemporary data sets compared to historic data sets. In three species, this loss was accompanied by a corresponding increase in inbreeding coefficient F_IS. We find that these genetic diversity declines correspond to declining contemporary effective population sizes (Ne) over deeper time scales, as well as fluctuations in contemporary estimates of Ne.

Conclusion: Our findings suggest that loss of genetic diversity resulting from historic population declines persists over time (50-100 years), even when population trajectories later stabilize. Our results highlight the utility of long-term genetic temporal comparisons to reveal hidden genetic diversity loss and reveal important considerations for managing genetic diversity loss.

Background: Organelle genome fragmentation is a drastic large-scale chromosomal mutation. Why and how organelle genomes become fragmented is still poorly understood. Two previous studies based on whole genome comparison between human louse and fruit fly proposed that the loss of mtSSB gene (for mitochondrial single-stranded DNA-binding protein) might be associated with mitochondrial (mt) genome fragmentation. Whether this association is valid has not been investigated due to the lack of mt genome fragmentation data.

Results: We investigated this association by exploring the genomic and transcriptomic data of 198 species of parasitic lice, book lice, bark lice, and other closely related hemipteroid insects accumulated in the past few decades. We show that the loss of mtSSB gene is correlated significantly with mt genome fragmentation in bark lice, book lice, and parasitic lice (Psocodea). The absence of mtSSB is more frequent than expected in the species with fragmented mt genomes whereas the presence of mtSSB is more frequent than expected in the species with single-chromosome mt genome organization. Nevertheless, our results reject a cause-and-effect relationship between the loss of mtSSB and mt genome fragmentation because mtSSB is present in 11 species of parasitic lice and one book louse species that have fragmented mt genomes.

Conclusions: The loss of mtSSB gene is correlated with mt genome fragmentation but is not the cause of mt genome fragmentation. Rather, it is plausible that fragmented mt genomes with multiple small-sized minichromosomes may make mtSSB gene and mtSSB protein less critical or unnecessary, leading to their loss eventually in the species with fragmented mt genomes.

Background: Accurate prediction of anticancer drug responses remains a significant challenge due to the intricate interplay between genomic features and pharmacological mechanisms. We present Matrix Completion with Low-rank Regularization and Principal Component Analysis (MCLRP), a multimodal framework that synergistically integrates low-rank matrix completion with transcriptomic principal component analysis through dual-stream feature interaction. This innovative architecture not only leverages the similarities among drugs and mutation patterns in cell lines via matrix completion but also preserves gene-level interpretability of response patterns by incorporating gene expression data into the model.

Results: Benchmarked against seven computational paradigms (including matrix completion, ridge regression, SRMF, and their hybrid variants) across the Genomics of Drug Sensitivity in Cancer (GDSC) and Cancer Cell Line Encyclopedia (CCLE) repositories, MCLRP demonstrated superior predictive performance for 75% of drug responses, alongside enhanced biological plausibility. Notably, the model identified imatinib as a potential therapeutic alternative for M14 melanoma cell lines through cross-drug response extrapolation, suggesting innovative strategies for overcoming doxorubicin resistance. Interestingly, our mutation-response mapping revealed that BRAF-mutated lineages exhibited a 4.7-fold increase in sensitivity (p < 1e-5) to AZ628 compared to wild-type lineages, with synergistic amplification (8.1-fold, p < 1e-7) observed in BRAF/PIK3CA co-mutants.

Conclusions: These findings establish MCLRP as a dual-purpose predictive-analytical tool that not only enhances drug response forecasting but also uncovers mutation-specific pharmacological vulnerabilities through systems-level pattern recognition.

Background: The interconnectedness of human, animal, and environmental health drives emerging threats, such as antimicrobial-resistant pathogens. The widespread use of the same antimicrobials in both human and livestock may play a role in interspecies bacterial transmission by disrupting natural microbial communities and creating an environment favouring resistant bacteria. Pigs and poultry receive high levels of antimicrobials and are reservoirs of multidrug-resistant bacteria, including Streptococcus suis, a zoonotic pig pathogen. S. suis detection in non-porcine hosts, particularly poultry, raises a critical question: is this due to transient spillover or does it represent sustained host jumps and adaptation?

Results: Analysing over 3000 S. suis genomes from a diverse range of hosts-including pigs, wild boar, humans, cats, dogs, cattle, fish, otter, and birds-we identify a multidrug-resistant lineage, distinct from the lineage responsible for most zoonoses, that has undergone multiple host jump events into birds. Unlike transmission to humans, which is exclusively derived through contacts with pigs, we find evidence of S. suis adaptation to birds. This includes phylogenetic persistence, independent acquisition of bird-specific mobile genomic islands, enhanced survival in chicken versus pig blood, and subsequent transmission from poultry to wild birds.

Conclusions: While chickens may not be a source of zoonotic S. suis infections, shared antibiotic usage in pigs and poultry may have promoted host jumps of multidrug-resistant S. suis, leading to onward transmission to wild bird populations. Our results suggest that antibiotic use in livestock production may promote transmission of antimicrobial-resistant bacteria to other hosts, thereby expanding the ecological range of bacterial pathogens.

Background: Based on the climate change and more extreme temperature events in the past 30 years, heat stress (HS) has become one of the most detrimental abiotic stresses that affect crop growth and development, limit their geographical distribution, and reduce yield. As a typical chimonophilous crop, wheat is very sensitive to high temperature. Deciphering the molecular mechanism of the wheat response to high temperature will help in the development of cultivars that perform better under HS.

Results: In this study, we identified a wheat Kelch-type F-box gene, TaFBK34. Overexpression of TaFBK34 wheat plants (TaFBK34-OE) showed stronger heat tolerance compared to the wild type, while plants with attenuated TaFBK34 (TaFBK34-RNAi) exhibited the phenotype of heat sensitivity. Increased expression of antioxidant-related genes and a heat-shock protein gene was observed in TaFBK34-OE plants compared with the wild type, coinciding with higher activities of the antioxidant enzymes, accumulation of proline and soluble sugar, reduced malondialdehyde and reactive oxygen species content. The opposite trends were observed in TaFBK34-RNAi lines. TaFBK34 interacts with the ADP-ribosylation factor, TaARL2. Compared to the wild type, more TaARL2 protein accumulated in TaFBK34-RNAi lines after HS treatment; moreover, TaARL2 continued to increase after MG132 (a proteasome inhibitor) injection for 12 h + 37 °C for 12 h, indicating that TaARL2 is involved in the response to HS and is degraded by the 26S proteasome.

Conclusions: These findings show that TaFBK34 improves wheat tolerance to HS, at least in part through an interaction with the TaARL2 protein, and provides potential applications of these genes for the improvement of wheat.

Background: The nervous system senses microbial signals to influence host defense. Pain-sensing nociceptor neurons are key regulators of the host response to infection, but how they perceive infections is not well understood. Using Caenorhabditis elegans as a tractable model host that shares many features with mammalian systems, we investigated the effects of infection on nociceptor function in vivo.

Results: In vivo intracellular Ca²⁺ imaging of C. elegans nociceptor ASH neurons revealed a drastic reduction in ASH responses to aversive stimuli in Staphylococcus aureus-infected animals compared to noninfected controls. Morphological examination revealed that ASH neurons lost integrity in the sensory processes reaching the mouth. Neighboring neurons did not show this pathogen-induced neurite pathology (PaIN) phenotype. During acute pathogen exposure, ASH neurons experience Ca²⁺ suppression. Genetic analysis indicated that apoptosis, necrosis, ferroptosis, and autophagy are not essential for the PaIN phenotype. Conversely, loss of the evolutionarily conserved stress-response transcription factor HLH-30/TFEB decreased the penetrance of ASH PaIN by approximately 50%. Additionally, infected animals exhibited defective ASH-mediated evasive behaviors, suggesting that the S. aureus-triggered reduction in ASH activation and morphological degeneration is physiologically relevant.

Conclusions: S. aureus damages nociceptor integrity in C. elegans: ASH neurons experience acute Ca²⁺ suppression-most pronounced with stationary-phase cultures-and extended exposure leads to structural damage and decreased avoidance behavior. This connection between pathogen physiology and circuit failure suggests that infection-evoked nociceptor PaIN may contribute to sensory dysfunction, highlighting the need to identify the responsible bacterial factor(s) and their host targets.

Background: The gut microbiota is essential for maintaining host homeostasis through its influence on metabolism, immunity, and neural signalling. Disruption of this microbial balance, known as gut dysbiosis, can alter gut-brain communication and has been associated with cognitive decline, with impairments in learning and memory. However, the cellular and molecular factors that lead to cognitive decline are not well understood. In this study we used an antibiotic-induced gut dysbiosis model.

Results: We observed that the animals with antibiotic-induced gut dysbiosis showed deficits in cognition, especially long-term memory consolidation. There was an increase in astrocytes and microglial activation in the CA1 subregion of the hippocampus. The microglia were observed to engage in synaptic pruning at the presynaptic terminals. This aberrant pruning might have disrupted synaptic plasticity and connectivity, contributing to the observed cognitive deficiency. CNTF was also observed to be elevated along with activation of the JAK/STAT3 pathway. CNTF can activate microglia. Our findings revealed that astrocytes, microglia, and CNTF form an inflammatory activation loop within the CA1 region of the hippocampus following antibiotic-induced gut dysbiosis.

Conclusions: In summary, our study demonstrates that antibiotic-induced gut dysbiosis triggers a cascade of neuroinflammatory events in the hippocampus, involving the elevation of CNTF, microglial pruning at presynaptic terminals, and reciprocal activation of glial cells, resulting in cognitive deficits. These findings highlight the critical role of gut-brain communication in maintaining neural homeostasis and identify CNTF as a potential therapeutic target for dysbiosis-associated cognitive disorders.