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Increasing vapor pressure deficit (VPD) increases atmospheric demand for water. While increased evapotranspiration (ET) in response to increased atmospheric demand seems intuitive, plants are capable of reducing ET in response to increased VPD by closing their stomata. We examine which effect dominates the response to increasing VPD: atmospheric demand and increases in ET or plant response (stomata closure) and decreases in ET. We use Penman‐Monteith, combined with semiempirical optimal stomatal regulation theory and underlying water use efficiency, to develop a theoretical framework for assessing ET response to VPD. The theory suggests that depending on the environment and plant characteristics, ET response to increasing VPD can vary from strongly decreasing to increasing, highlighting the diversity of plant water regulation strategies. The ET response varies due to (1) climate, with tropical and temperate climates more likely to exhibit a positive ET response to increasing VPD than boreal and arctic climates; (2) photosynthesis strategy, with C3 plants more likely to exhibit a positive ET response than C4 plants; and (3) plant type, with crops more likely to exhibit a positive ET response, and shrubs and gymniosperm trees more likely to exhibit a negative ET response. These results, derived from previous literature connecting plant parameters to plant and climate characteristics, highlight the utility of our simplified framework for understanding complex land‐atmosphere systems in terms of idealized scenarios in which ET responds to VPD only. This response is otherwise challenging to assess in an environment where many processes coevolve together. Plain Language Summary Plants can sense increasing dryness in the air and close up the pores on their leaves, preventing water loss. However, drier air also naturally demands more water from the land surface. Here we develop a simplified theory for when land surface water loss increases (atmospheric demand dominates) or decreases (plant response dominates) in response to increased dryness in the air. This theory provides intuition for how ecosystems regulate water in response to changes in atmospheric dryness. According to the theory, ecosystems are capable of broad range of behavior in response to increased atmospheric dryness, from strongly reducing water loss to allowing large increases in water loss. Ecosystem behavior depends both on environmental conditions and plant type. Key Points We derive a simplified analytical model for ecosystem‐scale evapotranspiration response to changes in vapor pressure deficit Ecosystems exhibit a range of behavior, from reductions to increases in evapotransipration, in response to increasing vapor pressure deficit The choice of stomatal conductance model fundamentally alters the relationship between evapotranspiration and vapor pressure deficit

Disulfidptosis, a regulated form of cell death, has been recently reported in cancers characterized by high SLC7A11 expression, including invasive breast carcinoma, lung adenocarcinoma, and hepatocellular carcinoma. However, its role in colon adenocarcinoma (COAD) has been infrequently discussed. In this study, we developed and validated a prognostic model based on 20 disulfidptosis-related genes (DRGs) using LASSO and Cox regression analyses. The robustness and practicality of this model were assessed via a nomogram. Subsequent correlation and enrichment analysis revealed a relationship between the risk score, several critical cancer-related biological processes, immune cell infiltration, and the expression of oncogenes and cell senescence-related genes. POU4F1, a significant component of our model, might function as an oncogene due to its upregulation in COAD tumors and its positive correlation with oncogene expression. In vitro assays demonstrated that POU4F1 knockdown noticeably decreased cell proliferation and migration but increased cell senescence in COAD cells. We further investigated the regulatory role of the DRG in disulfidptosis by culturing cells in a glucose-deprived medium. In summary, our research revealed and confirmed a DRG-based risk prediction model for COAD patients and verified the role of POU4F1 in promoting cell proliferation, migration, and disulfidptosis.

Pancreatic cancer (PC) is a highly lethal malignancy worldwide. Our previous study indicated that overexpression of USP34 could promote tumor growth in PC cells. Therefore, this study aimed to further investigate the role of USP34 during the tumorigenesis of PC. The level of USP34 in PANC-1 and MiaPaCa-2 cells transfected with USP34-shRNAs was detected by RT-qPCR. Moreover, transwell migration and Annexin V/PI analysis were conducted to detect cell migration and apoptosis, respectively. In this study, downregulation of USP34 markedly inhibited proliferation and migration, and induced apoptosis in PANC-1 cells. Moreover, silencing of USP34 obviously downregulated the levels of PRR11 and p-p38 in PANC-1 cells. An in vivo study in nude mice bearing PANC-1 cell xenografts confirmed these results. Downregulation of USP34 could inhibit proliferation and migration in PANC-1 cells via inhibiting PRR11, and inactivating p38 MAPK signaling. Therefore, USP34 might be a potential therapeutic target for the treatment of PC.

Mastitis is a common disease that hinders the development of dairy industry and animal husbandry. It leads to the abuse of antibiotics and the emergence of super drug-resistant bacteria, and poses a great threat to human food health and safety. Staphylococcus aureus ( S. aureus ) and Escherichia coli ( E. coli ) are the most common pathogens of mastitis in dairy cows and usually cause subclinical or clinical mastitis. CircRNAs and N 6 -methyladenosine (m 6 A) play important roles in immunological diseases. However, the mechanisms by which m 6 A modifies circRNA in bovine mammary epithelial cells remain poorly understood. The aim of our study was to investigate m 6 A-modified circRNAs in bovine mammary epithelial cells (MAC-T cells) injured by S. aureus and E. coli. The profile of m 6 A-modified circRNA showed a total of 1,599 m 6 A peaks within 1,035 circRNAs in the control group, 35 peaks within 32 circRNAs in the S. aureus group, and 1,016 peaks within 728 circRNAs in the E. coli group. Compared with the control group, 67 peaks within 63 circRNAs were significantly different in the S. aureus group, and 192 peaks within 137 circRNAs were significantly different in the E. coli group. Furthermore, we found the source genes of these differentially m 6 A-modified circRNAs in the S. aureus and E. coli groups with similar functions according to GO and KEGG analyses, which were mainly associated with cell injury, such as inflammation, apoptosis, and autophagy. CircRNA–miRNA–mRNA interaction networks predicted the potential circRNA regulation mechanism in S. aureus- and E. coli -induced cell injury. We found that the mRNAs in the networks, such as BCL2, MIF, and TNFAIP8L2, greatly participated in the MAPK, WNT, and inflammation pathways. This is the first report on m 6 A-modified circRNA regulation of cells under S. aureus and E. coli treatment, and sheds new light on potential mechanisms and targets from the perspective of epigenetic modification in mastitis and other inflammatory diseases.

E. coli is a ubiquitous pathogen that is responsible for over one million fatalities worldwide on an annual basis. In animals, E. coli can cause a variety of diseases, including mastitis in dairy cattle, which represents a potential public health hazard. However, the pathophysiology of E. coli remains unclear. We found that E. coli could induce global upregulation of m6A methylation and cause serious apoptosis in bovine mammary epithelial cells (MAC-T cells). Furthermore, numerous m6A-modified lncRNAs were identified through MeRIP-seq. Interestingly, we found that the expression of LOC4191 with hypomethylation increased in MAC-T cells upon E. coli-induced apoptosis. Knocking down LOC4191 promoted E. coli-induced apoptosis and ROS levels through the caspase 3–PARP pathway. Meanwhile, knocking down ALKBH5 resulted in the promotion of apoptosis through upregulated ROS and arrested the cell cycle in MAC-T cells. ALKBH5 silencing accelerated LOC4191 decay by upregulating its m6A modification level, and the process was recognized by hnRNP A1. Therefore, this indicates that ALKBH5 stabilizes m6A-modified LOC4191 to suppress E. coli-induced apoptosis. This report discusses an initial investigation into the mechanism of m6A-modified lncRNA in cells under E. coli-induced apoptosis and provides novel insights into infectious diseases.

Mastitis is one of the most common and significant infectious diseases in dairy cattle and is responsible for significant financial losses for the dairy industry globally. An important pathogen of bovine mastitis, Mycoplasma bovis ( M. bovis ) has a high infection rate, requires a long course of treatment, and is difficult to cure. Bovine mammary epithelial cells (BMECs) are the first line of defense of the mammary gland, and their natural immune system plays a critical role in resisting M. bovis infection. This study aimed to explore and demonstrate the regularity of Toll-like receptors (TLRs) activation during M. bovis infection and their function during M. bovis mastitis. An in vitro model of M. bovis -induced mastitis showed that the expression of IL-6, IL-8, and TNF-α increased significantly following infection. M. bovis infection also upregulated the expression of TLR1/2/6 on the cell membrane and TLR3/9 in the cytoplasm. There is a crosstalk effect between TLR1–TLR2 and TLR2–TLR6. Furthermore, M. bovis infection was found to activate the TLR1/2/6/9/MyD88/NF-κB and TLR3/TRIF/IRF signal transduction pathways, which in turn activate inflammatory factors. These findings lay the theoretical foundation for understanding the pathogenesis of M. bovis , permitting the development of effective measures for preventing and controlling M. bovis mastitis.

Escherichia coli and Staphylococcus aureus are two common pathogenic microorganisms that cause mastitis in dairy cows. They can cause clinical mastitis and subclinical mastitis. In recent studies, lncRNAs have been found to play an important role in the immune responses triggered by microbial inducers. However, the actions of lncRNAs in bovine mastitis remain unclear. The purpose of this study was to investigate the effects of bovine mammary epithelial cell injuries induced by treatment with E. coli and S. aureus, and to explore the lncRNA profile on cell injuries. The lncRNA transcriptome analysis showed a total of 2597 lncRNAs. There were 2234 lncRNAs differentially expressed in the E. coli group and 2334 in the S. aureus group. Moreover, we found that the E. coli and S. aureus groups of maternal genes targeted signaling pathways with similar functions according to KEGG and GO analyses. Two lncRNA–miRNA–mRNA interaction networks were constructed in order to predict the potential molecular mechanisms of regulation in the cell injuries. We believe that this is the first report demonstrating the dysregulation of lncRNAs in cells upon E. coli and S. aureus infections, suggesting that they have the potential to become important diagnostic markers and to provide novel insights into controlling and preventing mastitis.

N6-Methyladenosine (m6A) is the most abundant epigenetic RNA modification in eukaryotes, regulating RNA metabolism (export, stability, translation, and decay) in cells through changes in the activity of writers, erasers, and readers and ultimately affecting human life or disease processes. Inflammation is a response to infection and injury in various diseases and has therefore attracted significant attention. Currently, extensive evidence indicates that m6A plays an essential role in inflammation. In this review, we focus on the mechanisms of m6A in inflammatory autoimmune diseases, metabolic disorder, cardio-cerebrovascular diseases, cancer, and pathogen-induced inflammation, as well as its possible role as targets for clinical diagnosis and treatment.

Gliomas are highly invasive brain tumors in which metabolic reprogramming plays a pivotal role in tumor initiation and progression. METTL17, a mitochondria-associated methyltransferase, has been reported to enhance oxidative phosphorylation (OXPHOS) through mitochondrial RNA methylation; however, its function and regulatory mechanisms in glioma remain poorly understood. In this study, we manipulated METTL17 expression in primary P1 and U251 glioma cells using lentiviral-mediated knockdown and overexpression approaches. METTL17 depletion significantly suppressed cell proliferation, migration, and invasion, reduced ATP production and mitochondrial membrane potential, and increased reactive oxygen species accumulation, whereas METTL17 overexpression reversed these phenotypes. Mechanistically, METTL17 sustained mitochondrial OXPHOS by positively regulating key components of the electron transport chain, including NDUFA2, NDUFS1, SDHB, UQCRB, and MT-CO2. Mass spectrometry and co-immunoprecipitation analyses further revealed that METTL17 interacts with the E3 ubiquitin ligase RNF126, which destabilizes METTL17 through K116-dependent ubiquitination. Additionally, we demonstrate that SIRT5 acts as a desuccinylase for METTL17, removing succinylation at Lys274 and thereby facilitating RNF126-mediated ubiquitination and degradation of METTL17. In vivo xenograft experiments further validated that METTL17 knockdown markedly inhibited tumor growth and enhanced apoptosis. Collectively, these findings identify METTL17 as a critical regulator of mitochondrial function and energy metabolism in glioma and reveal a SIRT5-METTL17-RNF126 axis that governs METTL17 stability, providing new insights into glioma metabolic reprogramming and potential therapeutic targets.

Mastitis is a common disease in dairy cows that is mostly caused by E. coli, and it brings massive losses to the dairy industry. N6-Methyladenosine (m6A), a methylation at the N6 position of RNA adenine, is a type of modification strongly associated with many diseases. However, the role of m6A in mastitis has not been investigated. In this study, we used MeRIP-seq to sequence the RNA of bovine mammary epithelial cells treated with inactivated E. coli for 24 h. In this in vitro infection model, there were 16,691 m6A peaks within 7066 mRNA transcripts in the Con group and 10,029 peaks within 4891 transcripts in the E. coli group. Compared with the Con group, 474 mRNAs were hypermethylated and 2101 mRNAs were hypomethylated in the E. coli group. Biological function analyses revealed differential m6A-modified genes mainly enriched in the MAPK, NF-κB, and TGF-β signaling pathways. In order to explore the relationship between m6A and mRNA expression, combined MeRIP-seq and mRNA-seq analyses revealed 212 genes with concomitant changes in the mRNA expression and m6A modification. This study is the first to present a map of RNA m6A modification in mastitis treated with E. coli, providing a basis for future research.