Science China Life Sciences最新文献

Colpoda are among the most predominant eukaryotic microorganisms in soil ecosystems, playing crucial roles in material and energy cycling within soil and plant rhizosphere environments. Colpoda can form two distinct types of cysts in soil: reproductive cysts and resting cysts. Reproductive cyst represents an essential developmental stage for Colpoda proliferation and environmental adaptation. This study comprehensively characterized the reproductive cyst formation process of Colpoda inflata, identifying carbohydrate-coated granular structures derived from bacterial digestive products as their key morphological feature. C. inflata secretions were found to stimulate reproductive cyst formation effectively. We obtained a high-quality genome assembly of C. inflata and subsequently isolated and characterized three classes of excretory proteins. In vitro experiments demonstrated that an alpha-amylase is sufficient to induce reproductive cyst formation and rapid proliferation in a dose-dependent manner, achieving maximum cell densities 4.6 times higher than those in standard culture conditions. Further investigations revealed that C. inflata alpha-amylase could cross-induce reproductive cyst formation in different Colpoda species, with induction efficiency inversely correlated with phylogenetic distance. Heterologous expression of alpha-amylases from various Colpoda species demonstrated cross-induction capabilities, suggesting interspecies interactions among Colpodas in soil and rhizosphere ecosystems. In summary, this study provides critical insights into the molecular mechanisms underlying Colpoda reproductive cyst formation. The identified mechanism enables substantial biomass enhancement of Colpoda populations, allowing for future genetic engineering applications that aim to develop Colpoda-based bioremediation strategies for soil contaminants and microbial interventions in agricultural production systems.

Deep-sea hydrothermal vents are "extreme" environments with constantly fluctuating physicochemical conditions, but dense animal aggregations thrive primarily through symbiosis with chemoautotrophic bacteria to exploit the unusual chemistry. Alviniconcha snails, which harbor symbionts in their enlarged gill at an intermediate state between intracellular and extracellular, are a prime example. Here, we present chromosome-level genomes of two Alviniconcha species (A. adamantis and A. marisindica) to investigate the adaptations of this holobiont. Significant expansion of solute carrier families enhances nutrient transport between the two parties. Alviniconcha lacks complete methionine biosynthesis pathways, likely compensated by symbiont provisioning, highlighting host-symbiont metabolic complementarity. High myoglobin expression levels in the gills contradict previous reports of hemoglobin, suggesting myoglobin-mediated oxygen storage to mitigate fluctuating environmental oxygen levels. Spatial transcriptomics further delineated gill's functional zones on the gill filament responsible for symbiont digestion via phagocytosis in bacteriocytes, oxygen transport in secretory zones, and ciliary water flow regulation. Our findings elucidate molecular and physiological adaptations underpinning the Alviniconcha holobiont's success in dynamic vent ecosystems.

In angiosperms, fertilization recovery refers to the phenomenon wherein an ovule, upon failure of both sperm cells released by the initial pollen tube to achieve fertilization, continues to attract subsequent pollen tubes to salvage fertilization. Therefore, the efficiency of fertilization recovery is crucial for maximizing fertility. This efficiency primarily depends on the survival rate of the persistent synergid cell (PSC), which secretes pollen tube attractants. However, the relative contributions of the two fertilization events to PSC survival and subsequent fertilization recovery efficiency remain poorly understood. In this study, we utilized mutants defective in either double or single fertilization to assess PSC survival rates and fertilization recovery efficiency under different reproductive scenarios. By providing sufficient pollen through repeated pollination, we observed that the fertilization recovery efficiency in the double fertilization-defective mutant gcs1/hap2 increased from 75.7% to 97.4%, indicating that nearly all PSCs remain viable when double fertilization fails and highlighting the importance of timely and adequate pollen availability for fertilization recovery. Intriguingly, in mutants where egg cell fertilization failed, the PSC persisted in 48.2% of ovules, and about 43.1% of ovules attracted secondary pollen tubes. In contrast, in mutants where central cell fertilization failed, PSC persistence was observed in only 27.5% of the ovules, and fertilization recovery occurred in only 19.9%. These findings demonstrate that egg cell fertilization failure triggers significantly higher efficiency of fertilization recovery than central cell fertilization failure.

The intestinal epithelium is particularly vulnerable to oxidative stress caused by intracavitary stimulation, but the molecular mechanisms driving this damage remain poorly understood. The arachidonic acid (AA) pathway was significantly enriched in the transcriptome of in vivo oxidative stress-induced jejunum and in vitro oxidative stress-induced intestinal organoids, highlighting its critical role in mediating oxidative stress-induced epithelial injury. Additionally, oxidative stress elevated levels of AA in the jejunum in vivo, while the expression of genes related to epithelial differentiation, nutrient digestion, absorption, and transport was downregulated both in vivo and in AA-treated organoids in vitro. These findings indicated that oxidative stress disrupts intestinal epithelial cell differentiation through AA, leading to impaired intestinal function. Notably, inhibiting AA release not only enhanced organoid viability under oxidative stress but also reduced inflammatory responses in mice exposed to oxidative stress, demonstrating that AA serves as a key effector molecule in mediating oxidative stress-induced intestinal injury. By employing organoid models, this study clarified the pathological involvement of AA in oxidative stress-related intestinal injury, offering novel perspectives for potential therapeutic interventions in oxidative stress-associated gastrointestinal disorders.

Maternal fiber intake alters the maternal gut microbiota and metabolites, which benefits offspring health through unclear mechanisms. Using a sow model, the study showed that supplementing with purified fiber (cellulose:guar gum=3:1) increased weaning weight and resistance to LPS-induced intestinal injury. Milk analysis revealed higher levels of immunoglobulins and milk fat. Fecal microbiota transplantation (FMT) from fiber-fed sows to mice replicated these benefits, increasing milk fat, immunoglobulins, and pup growth. Akkermansia muciniphila (AKK) abundance was positively associated with milk quality in both models. Supplementing with AKK mimicked the effects of fiber, boosting milk fat and immunoglobulins. In in vitro experiments with HC11 mammary epithelial cells showed that AKK metabolites enhanced milk fat synthesis and immunoglobulin transporter expression. Metabolite analysis indicated that AKK influences mammary gland function by increasing acetate and propionate levels, with acetate promoting milk fat synthesis via GPR43 and propionate regulating immunoglobulin transport through GPR41. Therefore, maternal fiber intake promotes intestinal AKK abundance, increases short-chain fatty acids (SCFAs) production, and influences lactation via GPR41/43 signaling.

Mitochondria, serving as the energy hub and death-immune hub of cells, play pivotal roles in maintaining normal cellular physiology and pathological functions. Under stress conditions, mitochondria can be released from cells into the extracellular environment and even the circulatory system through multiple pathways, and subsequently taken up by other cells. The process of mitochondrial release involves complex mechanisms, exerting multifaceted effects on the fate and functions of recipient cells and playing critical roles in both physiological and pathological processes. This review focuses on the stress-induced release of mitochondria, their uptake by recipient cells, and the changes brought about in the peripheral circulation, aiming to deepen the understanding of the molecular mechanisms and biological implications of this novel mode of intercellular communication and provide new therapeutic insights for related diseases.

Mechanical signaling plays a crucial yet poorly understood role in human neural tube morphogenesis. In this study, we elucidate how the Hippo pathway mechanosensor YAP converts apical tension into transcriptional programs to guide this process. Using human cortical organoids, we demonstrated that YAP accumulates and translocates to the nucleus within high-tension apical domains of neural rosettes. YAP depletion disrupted apicobasal epithelial polarity, manifested as disorganized cytoskeleton, compromised tight junctions, and impaired ciliogenesis, which ultimately resulted in defective rosette morphogenesis. Mechanistically, the YAP-TEAD4 complex transcriptionally activated LEF1, a central regulator of Wnt signaling. LEF1 deficiency phenocopied YAP loss, whereas its overexpression partially rescued rosette defects. Our findings establish the YAP-LEF1 axis as a critical integrator of mechanical and morphogenetic signals in neural tube development, thereby highlighting its potential as a therapeutic target for neural tube defects such as anencephaly.