Core Viewpoint - The current pathogen surveillance system primarily focuses on livestock and companion animals, neglecting non-traditional livestock and wild mammals, which poses a risk for cross-species transmission of pathogens and antibiotic resistance genes [2][3]. Group 1: Research Findings - A study published in the journal Cell identified a significant number of unrecorded viruses and bacteria in asymptomatic mammals, revealing extensive cross-species transmission [3][4]. - The research analyzed samples from 973 asymptomatic mammals, identifying 128 virus species (30 of which are newly discovered), 10,255 bacterial species (over 7,000 previously uncharacterized), 201 fungi, and 7 parasites [4][6]. - The study found that 13.3% of virus species coexisted in both farmed and wild mammals, including canine coronavirus in Asian black bears and Getah virus in rabbits [4][6]. Group 2: Antibiotic Resistance Insights - The research team observed 157 clinically significant antibiotic resistance genes (ARGs) in the microbiomes of farmed and wild mammals, with over 99% homology to ARGs found in human microbiomes [4][6]. - The presence of mobile genetic elements (MGE) alongside ARGs suggests a potential reservoir of antibiotic resistance in animal microbiomes, which could accelerate cross-species transmission due to antibiotic misuse [6][7]. Group 3: Implications for Public Health - The findings indicate that asymptomatic animals may serve as potential hosts for novel zoonotic viruses, highlighting the need for systematic monitoring of pathogens and antibiotic resistance genes at the "animal-environment-human" interface [6][7].

Core Insights - The article discusses the significant advancements in the understanding of migrasomes, a newly discovered organelle, over the past decade, highlighting their biological roles and implications in various diseases [2][3]. Summary by Sections Discovery and Characteristics of Migrasomes - In 2015, a team led by Professor Yu Li at Tsinghua University identified migrasomes in NRK cells, which are large membrane-bound structures resembling open pomegranates, crucial for cell migration [5]. - Migrasomes contain numerous internal vesicles and are rich in specific proteins, indicating their complex structure and dual role as both secretion hubs and extracellular vesicles [5][6]. Mechanisms of Biogenesis - The biogenesis of migrasomes occurs in three stages: nucleation triggered by SMS2 spots, maturation coordinated by the PIP5K1α-Rab35-integrin signaling axis, and expansion facilitated by the formation of a specialized microdomain [13]. Physiological Functions - Migrasomes participate in various physiological processes, including local secretion of signaling molecules, targeted protein and RNA transfer between adjacent cells, and maintenance of cellular homeostasis under stress [18]. Challenges in Research - Current methods for detecting and analyzing migrasomes are limited, necessitating advancements in microscopy and the development of reliable animal models for accurate labeling [19][20]. - Fundamental questions regarding the cellular origin, abundance, distribution, and dynamics of migrasomes remain unanswered, indicating a need for collaborative research efforts [21]. Implications in Disease - Migrasomes are believed to play significant roles in various diseases, particularly in immune-related conditions, suggesting potential avenues for further research [24]. - The therapeutic potential of migrasomes is highlighted, as they could serve as diagnostic tools or delivery vehicles for treatments, marking a transformative shift in the field [24].

Core Viewpoint - The study reveals that the oligomerization of Shank3 regulates the material properties of postsynaptic density (PSD) condensates, which are crucial for synaptic plasticity and neuronal functions related to learning and memory [3][5][7]. Summary by Sections - The research team from Southern University of Science and Technology published findings indicating that PSD condensates exhibit soft-glass-like properties, with Shank3 protein oligomerization playing a key role in governing these material characteristics [3][5]. - The study found that the reconstructed PSD condensates formed a soft-glass material without signs of irreversible amyloid-like structures. This glass-like formation relies on specific, multivalent interactions among scaffold proteins, which mediate the network flow of PSD proteins [4]. - Disruption of Shank3's SAM domain-mediated oligomerization, observed in patients with Phelan-McDermid syndrome, leads to a softening of PSD condensates, impairing synaptic transmission and plasticity, and resulting in autism-like behaviors in mice [4][5]. - Overall, the research emphasizes the importance of the material properties of PSD condensates in neuronal synaptic functions related to learning and memory [7].

Core Viewpoint - The research reveals that aggresomes, a type of non-membrane organelle in Escherichia coli, play a crucial role in protecting mRNA integrity under stress, thereby enhancing bacterial survival and recovery efficiency in adverse conditions [4][7][9]. Group 1: Research Findings - The study published in Nature Microbiology demonstrates that aggresomes selectively protect mRNA through electrostatic repulsion mechanisms, which is vital for the survival of persister cells under stress [4][8]. - Long-term stress leads to ATP depletion, resulting in increased formation and accumulation of aggresomes, along with specific mRNA enrichment within these structures [8]. - The research indicates that mRNA stored in aggresomes facilitates rapid reactivation of translation, contributing to a reduction in lag phase during bacterial growth after stress removal [8][9]. Group 2: Implications - Understanding the role of aggresomes in mRNA protection provides insights into bacterial resistance mechanisms, potentially guiding the development of novel antibacterial strategies targeting persister cells [4][7]. - The findings highlight the significance of non-membrane organelles in bacterial stress responses, which could influence future research in microbiology and antibiotic resistance [4][9].

Core Viewpoint - The research published by Tsinghua University's team reveals a unique "hypertranscription state" in early embryos, highlighting the interplay between chromatin architecture and transcriptional activity, indicating a highly coordinated interaction between chromatin structure and transcription processes [2][5]. Group 1: Chromatin Structure and Dynamics - The study identifies that the conventional chromatin organization, including Topologically Associating Domains (TADs), disassembles after fertilization, followed by a slow re-establishment of three-dimensional chromatin structure during zygotic genome activation [2]. - CTCF, a highly conserved DNA-binding protein, plays a crucial role in regulating chromatin higher-order structures and is continuously present in chromatin during early mouse development, while cohesin's binding ability is weak during the single-cell embryo stage [4]. Group 2: Gene Activation and Cohesin Islands - The research found that genes associated with Genic Cohesin Islands (GCIs) are enriched in cell identity and regulatory genes, showing extensive H3K4me3 modifications in their promoter regions, indicating active transcription [5]. - There is a significant transcriptional activity from the two-cell to the eight-cell stage, which is essential for GCI formation, and induced transcription can directly generate GCIs [5]. Group 3: Interaction Between Chromatin and Transcription - GCIs serve as insulating boundaries that form contact domains with adjacent CTCF sites, enhancing both the transcription levels and stability of GCI-related genes [5]. - The findings emphasize the dynamic remodeling of three-dimensional genome structures and their reciprocal regulation by transcriptional activity, underscoring the close relationship between chromatin conformation and transcription processes in early embryos [5].

Core Viewpoint - The research highlights the evolutionary adaptation mechanisms in skin that support terrestrial locomotion, particularly focusing on the role of the SLURP1 gene in preventing palmoplantar keratoderma (PPK) [2][3]. Group 1: Evolutionary Mechanisms - The transition from aquatic to terrestrial life required vertebrates to overcome significant physiological and biomechanical challenges, with skin structure being crucial for this adaptation [2]. - The study published in Cell reveals a mechano-resistance mechanism in skin that adapts to the mechanical stresses of land locomotion [2][5]. Group 2: SLURP1 Gene and PPK - The SLURP1 gene is specifically expressed in the skin of the palms and soles of four-legged animals, and mutations in this gene in humans lead to PPK, characterized by excessive thickening and cracking of the skin [3][6]. - In SLURP1 knockout mice, reducing mechanical stress on the paw skin completely reverses the PPK phenotype, indicating the gene's critical role in skin health [3][6]. Group 3: Mechanistic Insights - SLURP1 protein is located in the endoplasmic reticulum (ER) membrane and interacts with the calcium pump SERCA2b, maintaining calcium levels under mechanical stress [3][6]. - By regulating the activity of SERCA2b, SLURP1 prevents the activation of the pPERK-NRF2 signaling pathway, which is associated with PPK, thus maintaining epidermal homeostasis [3][6].

Core Viewpoint - The recent research published in PNAS by a team from Westlake University reveals the structural basis of auxin binding and transport by the AUX1 protein in Arabidopsis thaliana, which is crucial for understanding plant growth and development [2][5]. Group 1: Research Findings - The study elucidates the cryo-electron microscopy structures of AUX1 in both IAA-unbound and IAA-bound states, highlighting the significant conformational changes that occur upon IAA binding [3][5]. - AUX1 exists as a monomer and comprises 11 transmembrane helices, with TM1 to TM5 and TM6 to TM10 forming two halves of the classic LeuT fold, while TM11 interacts at the junction of these halves [5]. - The central pocket formed by TM1, TM3, TM6, and TM8 specifically recognizes IAA, and the conformational changes in TM1 and TM6 are critical for the transport of IAA [5]. Group 2: Implications and Future Research - The findings provide a molecular basis for AUX1-mediated IAA binding and transport, laying the groundwork for future structural-based functional studies of the AUX1/LAX family and the application of auxin analogs in agriculture [5]. - Following the PNAS publication, a related study from institutions in France, Denmark, and Germany was published in Nature Plants, which also analyzed the structures and mechanisms of AUX/LAX transporters involved in auxin import [6].

Core Viewpoint - The article discusses recent research that uncovers the biosynthesis pathway of salicylic acid in plants, which is crucial for their defense mechanisms and has implications for developing disease-resistant crop varieties [4][14][20]. Group 1: Research Findings - A team from Sichuan University published a study in Nature revealing a three-step biosynthesis pathway of salicylic acid from benzoyl-CoA in plants [4][5]. - The study identified three key enzymes involved in this pathway: BEBT, BBO, and BSH, which are conserved across various plant species [13][14]. - The research provides a molecular basis for understanding the differences in disease resistance among different plant groups, particularly major food crops [6][14]. Group 2: Comparative Studies - Concurrently, two other studies from Zhejiang University and Zhejiang Normal University also published in Nature focused on the biosynthesis of salicylic acid from phenylalanine, contributing to a more comprehensive understanding of this process [16][18][20]. - These studies collectively address the long-standing gaps in knowledge regarding salicylic acid biosynthesis pathways in plants [20].

Core Viewpoint - The article discusses a groundbreaking study that constructs a comprehensive human proteome aging map across a 50-year lifespan, revealing critical insights into the molecular mechanisms of aging and potential intervention targets [3][4][19]. Group 1: Research Findings - The study integrates ultra-sensitive mass spectrometry and machine learning to create a dynamic landscape of protein aging across seven physiological systems and 13 key tissues [4]. - It identifies protein information disruption as a core feature of organ aging, highlighting the role of mRNA-protein decoupling and pathological amyloid deposition in the systemic collapse of proteostasis networks [7]. - The vascular system is established as a "pioneer organ" in the aging process, significantly deviating from homeostatic trajectories early in life [7]. Group 2: Molecular Characterization of Aging - The research confirms that aging is accompanied by systemic proteostasis imbalance, characterized by a breakdown of the central dogma information flow, leading to impaired conversion of genetic information into functional proteins [9]. - Key findings include widespread accumulation of pathological proteins, forming an inflammatory aging network, which serves as a molecular basis for inflammaging [9][10]. Group 3: Aging Milestones and Mechanisms - The study identifies around 30 years of age as a critical inflection point for aging trajectories, with adrenal tissues showing early aging characteristics [12]. - A significant biological transition occurs between 45-55 years, where most organ proteomes experience a "molecular cascade storm," marking a key window for systemic aging acceleration [12][21]. Group 4: Vascular Aging Mechanisms - The research validates the "vascular aging hub" hypothesis, demonstrating that specific senescence-associated secretory factors, such as GAS6, drive endothelial and smooth muscle cell aging [15][16]. - Evidence supports the theory of "aging diffusion," where local aging tissues influence distant organs through specific secretory factors [16]. Group 5: Implications for Aging Research and Interventions - The study proposes a new framework for systemic aging research, moving beyond single-tissue models to a multi-organ interaction network [19]. - It introduces a novel tool for precise aging assessment through the development of organ-specific "proteome aging clocks," enabling non-invasive evaluation of biological age [20]. - Key intervention targets are identified, including factors mediating inter-organ signaling and common biomarkers, with the 45-55 age range highlighted as a critical intervention window [21]. - The findings pave the way for proactive aging disease prevention strategies, shifting from reactive treatment to early intervention based on molecular aging clocks [23]. Group 6: Methodological Innovations - The research successfully combines ultra-sensitive mass spectrometry, AI modeling, and multi-scale omics analysis to create a comprehensive framework for studying aging [24]. - This methodological advancement enhances the understanding of human aging and accelerates the translation of life sciences technologies into clinical applications [24].

Core Findings - The study reveals a "same-sex clustering" phenomenon in families with multiple children, challenging the traditional view that each child's gender is an independent event with a 50% probability for boys and girls [3][4][5][7] - For families with three or more children, the likelihood of having all boys or all girls is higher than having both genders [7] - The probability of a woman having another boy after already having one boy is 57%, and this probability increases to 61% after having three boys. Similarly, the probability of having another girl after having one girl is 53%, increasing to 58% after three girls [4][5] Maternal Age Influence - The research indicates that a mother's age at the time of her first childbirth significantly affects the gender of her children. Women who give birth after the age of 29 have a 13% higher probability of having only boys or only girls compared to those who give birth before age 23 [9][10] - This suggests that the maternal environment, which changes with age, may influence the success of sperm carrying X or Y chromosomes [10] Genetic Factors - The study identifies specific genes associated with a tendency to give birth to boys or girls. A particular SNP (rs58090855) on chromosome 10 is linked to a higher likelihood of having girls, while another SNP (rs1506275) near the TSHZ1 gene on chromosome 18 is associated with a higher likelihood of having boys [12][13] - This indicates that some women may have a genetic predisposition that affects the gender ratio of their offspring, providing a new perspective on family gender patterns [13] Conclusion - Overall, the research demonstrates that the gender of newborns is not entirely random, with maternal age and specific genetic mutations playing significant roles in determining offspring gender [14][15] - The findings open new avenues for exploring the complex biological mechanisms influencing gender determination, while emphasizing that the study's purpose is to reveal natural patterns rather than to facilitate gender selection [15][16]