Stress-induced Growth Research Articles

ETHYLENE RESPONSE FACTOR6, A Central Regulator of Plant Growth in Response to Stress.

ETHYLENE RESPONSE FACTOR6 (ERF6) has emerged as a central player in stress-induced plant growth inhibition. It orchestrates complex pathways that enable plants to acclimate and thrive in challenging environments. In response to various abiotic and biotic stresses, ERF6 is promptly activated through both ethylene-dependent and -independent pathways, and contributes to enhanced stress tolerance mechanisms by activating a broad spectrum of genes at various developmental stages. Despite the crucial role of ERF6, there is currently a lack of published comprehensive insights into its function in plant growth and stress response. In this respect, based on the tight connection between ethylene and ERF6, we review the latest research findings on how ethylene regulates stress responses and the mechanisms involved. In addition, we summarize the trends and advances in ERF6-mediated plant performance under optimal and stressful conditions. Finally, we also highlight key questions and suggest potential paths to unravel the ERF6 regulon in future research.

Stress-Induced Sulfide Production by Bacillus subtilis and Bacillus megaterium.

It was previously discovered that, in the Gram-negative bacterium Escherichia coli growing on a minimal medium with sulfate, stress-induced growth arrest is accompanied by the release of hydrogen sulfide. The source of the sulfide is the desulfurization of intracellular cysteine as one of the ways of maintaining it at a safe level. The danger of excess cysteine is associated with its participation in the Fenton reaction, leading to the formation of highly toxic hydroxyl radicals. Using electrochemical sensors, we identified stress-induced sulfide production in the Gram-positive bacteria Bacillus subtilis and Bacillus megaterium, growing on a minimal medium with sulfate, and changes in physiological parameters such as Eh, pH, and oxygen and potassium consumption. Sulfide production was observed during growth arrest due to the depletion of glucose, ammonium or antibiotic action. The use of sensors allowed to continuously record, in growing cultures, even small changes in parameters. There were significant differences in the amount and kinetics of sulfide production between Bacillus and E. coli. These differences are thought to be due to the lack of glutathione in Bacillus. It is suggested that stress-induced sulfide production by Bacillus under the described conditions may be one of the previously unknown sources of hydrogen sulfide in nature.

Dynamics of Actin Filaments Play an Important Role in Root Hair Growth under Low Potassium Stress in Arabidopsis thaliana.

Potassium (K) is an essential nutrient for the growth and development of plants. Root hairs are the main parts of plants that absorb K+. The regulation of plant root hair growth in response to a wide range of environmental stresses is crucially associated with the dynamics of actin filaments, and the thick actin bundles at the apical and sub-apical regions are essential for terminating the rapid elongation of root hair cells. However, the dynamics and roles of actin filaments in root hair growth in plants' response to low K+ stress are not fully understood. Here, we revealed that root hairs grow faster and longer under low K+ stress than the control conditions. Compared to control conditions, the actin filaments in the sub-apex of fast-growing wild-type root hairs were longer and more parallel under low K+ stress, which correlates with an increased root hair growth rate under low K+ stress; the finer actin filaments in the sub-apex of the early fully grown Col-0 root hairs under low K+ stress, which is associated with low K+ stress-induced root hair growth time. Further, Arabidopsis thaliana actin bundling protein Villin1 (VLN1) and Villin4 (VLN4) was inhibited and induced under low K+ stress, respectively. Low K+ stress-inhibited VLN1 led to decreased bundling rate and thick bundle formation in the early fully grown phase. Low K+ stress-induced VLN4 functioned in keeping long filaments in the fast-growing phase. Furthermore, the analysis of genetics pointed out the involvement of VLN1 and VLN4 in the growth of root hairs under the stress of low potassium levels in plants. Our results provide a basis for the dynamics of actin filaments and their molecular regulation mechanisms in root hair growth in response to low K+ stress.

Isolation and assessment of the beneficial effect of exopolysaccharide-producing PGPR in Triticum aestivum (L.) plants grown under NaCl and Cd -stressed conditions

Exopolysaccharide (EPS)-producing beneficial bacteria play a multifaceted role in improving plant growth and adaptive responses against different stressors. In this study, we isolated 25 bacterial strains from pea nodules and were further studied for their sodium chloride (NaCl) and cadmium (Cd) stress tolerance. Based on our results, Rhizobium fabae SR-22 (NCBI Accession number: MG063739.1) showed better tolerance toward salinity and Cd stress and produced a wide range of plant growth-promoting compounds. However, the amount of EPS varies during NaCl and Cd stress. It was important to note that NaCl and Cd beyond the tolerant level, affected the morphology and cellular viability of R. fabae. Interestingly, plant growth-promoting (PGP) substances (indole-3-acetic acid, ammonia, siderophore, and ACC deaminase) released by R. fabae were increased with increasing NaCl concentrations. In contrast, PGP substances were greatly decreased by increasing Cd dosages. Further, the beneficial effect of EPS-producing R. fabae in Triticum aestivum grown in soil treated with different levels of NaCl and Cd was assessed. Inoculation of R. fabae in wheat seedlings grown under higher NaCl and Cd concentrations showed improved growth compared to non-inoculated plants. R. fabae exhibited maximum effect in wheat plants grown under 2% NaCl and increased seed germination (8%), root length (13%), vigor indices (19%), root biomass (20%), chlorophyll-a (31%), total chlorophyll (27%) and carotenoid content. Additionally, R. fabae increased Cd and NaCl tolerance in wheat seedlings and improved their antioxidative responses. Conclusively, this work demonstrated that EPS-producing R. fabae showed a promising role in mitigating salinity and Cd-stress in wheat possibly by reducing salt and HM stress-induced abrasions and growth promotion via inorganic phosphate solubilization, and increased nutrient absorption. In the future, R. fabae equipped with these distinguishing characteristics may be used as effective bio-inoculants/bio-formulations in agriculture to address salinity and HM stress issues.

Mechanical stress-induced connective tissue growth factor plays a critical role in intestinal fibrosis in Crohn's-like colitis.

Crohn's disease (CD) is an inflammatory bowel disease characterized by transmural inflammation and intestinal fibrosis. Mechanisms of fibrosis in CD are not well understood. Transmural inflammation is associated with inflammatory cell infiltration, stenosis, and distention, which present mechanical stress (MS) to the bowel wall. We hypothesize that MS induces gene expression of profibrotic mediators such as connective tissue growth factor (CTGF), which may contribute to fibrosis in CD. A rodent model of CD was induced by intracolonic instillation of TNBS to the distal colon. TNBS instillation induced a localized transmural inflammation (site I), with a distended colon segment (site P) proximal to site I. We detected significant fibrosis and collagen content not only in site I but also in site P in CD rats by day 7. CTGF expression increased significantly in sites P and I, but not in the segment distal to the inflammation site. Increased CTGF expression was detected mainly in the smooth muscle cells (SMCs). When rats were fed exclusively with clear liquid diet to prevent mechanical distention in colitis, expression of CTGF in sites P and I was blocked. Direct stretch led to robust expression of CTGF in colonic SMC. Treatment of CD rats with anti-CTGF antibody FG-3149 reduced fibrosis and collagen content in both sites P and I and exhibited consistent trends toward normalizing expression of collagen mRNAs. In conclusion, our studies suggest that mechanical stress, by upregulating profibrotic mediators, i.e., CTGF, may play a critical role in fibrosis in CD.NEW & NOTEWORTHY We found that CTGF expression increased significantly not only in the inflammation site but in the distended segment proximal to inflammation in a rodent model of CD-like colitis. Release of mechanical distention prevented CTGF expression in CD rats, whereas direct stretch induced CTGF expression. Treatment with anti-CTGF antibody reduced fibrosis and collagen contents in CD rats. Thus, mechanical stress, via upregulating profibrotic mediators, i.e., CTGF, may play a critical role in fibrosis in CD.

Arnicolide D Inhibits Oxidative Stress-induced Breast Cancer Cell Growth and Invasion through Apoptosis, Ferroptosis, and Parthanatos.

Breast cancer is the most common malignant tumor in women, and its pathogenesis is very complicated. More and more studies have found that Traditional Chinese Medicine plays an important role in tumor prevention. To investigate the mechanism of arnicolide D isolated from Centipeda minima in breast cancer. Cell Counting Kit-8 (CCK-8), western blot, RT-qPCR, ELISA, flow cytometry, and Transwell were used to detect the effect of arnicolide D on the biological function of breast cancer cells. Arnicolide D promoted reactive oxygen species (ROS) production and induced a decrease in mitochondrial membrane potential in breast cancer cells, thereby inhibiting cell viability and increasing lactate dehydrogenase (LDH) release. Arnicolide D activated the classical apoptosis pathway to induce cell apoptosis; it significantly promoted PARP-1 expression, enhanced the nuclear translocation of apoptosis-inducing factor (AIF), and reduced the expression of AIF in mitochondria, indicating that it can induce the occurrence of parthanatos in a ROS dependent manner. In addition, arnicolide D down-regulated glutathione peroxidase 4 (GPX4) expression and increased the accumulation of Fe2+ and malondialdehyde (MDA), thereby activating ferroptosis. Apoptosis inhibitor, ferroptosis inhibitor, PARP inhibitor, PARP-1 siRNA, AIF siRNA and GPX4 overexpression vector significantly attenuated the inhibitory effect of arnicolide D on cell viability and reduced LDH release, which indicates that arnicolide D inhibits breast cancer cell growth by inducing apoptosis, parthanatos and ferroptosis. Arnicolide D also reduced breast cancer cell invasion and inhibited the expression of matrix metallopeptidase (MMP)-2 and MMP-9. Arnicolide D can activate a variety of cell death modes by inducing oxidative stress, thereby inhibiting the growth and invasion of breast cancer cells, indicating that arnicolide D has a good anti-tumor effect.

Quercetin inhibits chronic stress-mediated progression of triple-negative breast cancer by blocking β2-AR/ERK1/2 pathway

Chronic stress-mediated sustained release of neurotransmitters, which ultimately leads to the activation of β2-adrenergic receptor (β2-AR) signaling, is one of the most important reasons for triple-negative breast cancer (TBNC) progression. Quercetin (Que) has been proven to have the advantage of ameliorating stress psychological disorder. Our present study aimed to investigate the effect of Que on tumor growth and metastasis in TNBC xenograft mice undergoing stress, and to explore its underlying mechanisms. We first evaluated the effect of Que on the progression of TNBC in nude mice in vivo. The results showed that, Que could inhibit chronic stress-induced TNBC growth and occurrence of lung metastasis. We subsequently employed epinephrine (E) as a representative of stress hormone to investigate its possible mechanism in vitro. The results showed that, Que could inhibit E-mediated proliferation and migration of TNBC cells by blocking β2-AR/ERK1/2 pathway. In conclusion, our data demonstrated that Que could inhibit chronic stress-induced ERK1/2 activity in TNBC cells, and thereby weakening the potential for TNBC growth and metastasis.

Overexpression of acdS in petunia reduces ethylene production and improves tolerance to heat stress.

Petunia hybrida, widely grown as a bedding plant, has reduced growth and flower quality at temperatures above 30 °C (heat stress), primarily due to heat stress-induced ethylene (ET) production. The gene acdS encodes the 1-aminocyclopropane-1-carboxylate (ACC) deaminase (ACCD) enzyme, which is known for its role in reducing ET production by breaking down the ET precursor, ACC, in plant tissues. This study investigated the impact of heat stress on both 'Mirage Rose' WT petunia and its acdS-overexpressing transgenic lines. Heat stress-induced growth inhibition was observed in WT plants but not in transgenic plants. The increased stress tolerance of transgenic plants over WT plants was associated with lower ET production, ROS accumulation, higher SPAD values, water content, and relative water content. Furthermore, higher sensitivity of the WT to heat stress than the transgenic plants was confirmed by analysing ET signalling genes, heat shock transcription factor genes, and antioxidant- and proline-related genes, more strongly induced in WT than in transgenic plants. Overall, this study suggests the potential application of acdS overexpression in other floriculture plants as a viable strategy for developing heat stress-tolerant varieties. This approach holds promise for advancing the floricultural industry by overcoming challenges related to heat-induced growth inhibition and loss of flower quality.

Potential utility of l-carnitine for preventing liver tumors derived from metabolic dysfunction-associated steatohepatitis.

Recent reports have unveiled the potential utility of l-carnitine to alleviate metabolic dysfunction-associated steatohepatitis (MASH) by enhancing mitochondrial metabolic function. However, its efficacy at preventing the development of HCC has not been assessed fully. l-carnitine (2g/d) was administered to 11 patients with MASH for 10 weeks, and blood liver function tests were performed. Five patients received a serial liver biopsy, and liver histology and hepatic gene expression were evaluated using this tissue. An atherogenic plus high-fat diet MASH mouse model received long-term l-carnitine administration, and liver histology and liver tumor development were evaluated. Ten-week l-carnitine administration significantly improved serum alanine transaminase and aspartate transaminase levels along with a histological improvement in the NAFLD activity score, while steatosis and fibrosis were not improved. Gene expression profiling revealed a significant improvement in the inflammation and profibrotic gene signature as well as the recovery of lipid metabolism. Long-term l-carnitine administration to atherogenic plus high-fat diet MASH mice substantially improved liver histology (inflammation, steatosis, and fibrosis) and significantly reduced the incidence of liver tumors. l-carnitine directly reduced the expression of the MASH-associated and stress-induced transcriptional factor early growth response 1. Early growth response 1 activated the promoter activity of neural precursor cell expressed, developmentally downregulated protein 9 (NEDD9), an oncogenic protein. Thus, l-carnitine reduced the activation of the NEDD9, focal adhesion kinase 1, and AKT oncogenic signaling pathway. Short-term l-carnitine administration ameliorated MASH through its anti-inflammatory effects. Long-term l-carnitine administration potentially improved the steatosis and fibrosis of MASH and may eventually reduce the risk of HCC.

Ganoderma lucidum extract attenuates corticotropin-releasing hormone-induced cellular senescence in human hair follicle cells

Corticotropin-releasing hormone (CRH) is a key mediator in stress-induced hair growth inhibition. Here, we investigated the impact of stress-induced senescence and evaluated the potential of Ganoderma lucidum (GL) extract in mitigating CRH-induced senescence in human hair follicle cells (hHFCs). We show that CRH treatment increased the senescence-associated beta-galactosidase (SA-β-GAL) activity and reactive oxygen species (ROS) formation in hHFCs and suppressed alkaline phosphatase (ALP) activity and anagen-inducing genes. However, GL extract restored ALP activity and decreased the expression levels of anagen-related genes in CRH-treated hHFCs. It decreased SA-β-GAL activity, reduced ROS production, and prevented the phosphorylation of MAPK signaling pathways in CRH-related stress response. Moreover, GL reversed the CRH-induced inhibition of two-cell assemblage (TCA) elongation and Ki67 expression. GL extract attenuates stress-induced hair follicular senescence by delaying catagen entry and scavenging ROS. Our findings suggest that GL extract could be used for treating stress-induced hair loss.

Methylmercury Induces Apoptosis in Mouse C17.2 Neural Stem Cells through the Induction of OSGIN1 Expression by NRF2.

Methylmercury is a known environmental pollutant that exhibits severe neurotoxic effects. However, the mechanism by which methylmercury causes neurotoxicity remains unclear. To date, we have found that oxidative stress-induced growth inhibitor 1 (OSGIN1), which is induced by oxidative stress and DNA damage, is also induced by methylmercury. Therefore, in this study, we investigated the relationship between methylmercury toxicity and the induction of OSGIN1 expression using C17.2 cells, which are mouse brain neural stem cells. Methylmercury increased both OSGIN1 mRNA and protein levels in a time- and concentration-dependent manner. Moreover, these increases were almost entirely canceled out by pretreatment with actinomycin D, a transcription inhibitor. Furthermore, similar results were obtained from cells in which expression of the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) was suppressed, indicating that methylmercury induces OSGIN1 expression via NRF2. Methylmercury causes neuronal cell death by inducing apoptosis. Therefore, we next investigated the role of OSGIN1 in methylmercury-induced neuronal cell death using the activation of caspase-3, which is involved in apoptosis induction, as an indicator. As a result, the increase in cleaved caspase-3 (activated form) induced by methylmercury exposure was decreased by suppressing OSGIN1, and the overexpression of OSGIN1 further promoted the increase in cleaved caspase-3 caused by methylmercury. These results suggest, for the first time, that OSGIN1 is a novel factor involved in methylmercury toxicity, and methylmercury induces apoptosis in C17.2 cells through the induction of OSGIN1 expression by NRF2.

Multi-scaled temporal modeling of cardiovascular disease progression: An illustration of proximal arteries in pulmonary hypertension

The progression of cardiovascular disease is intricately influenced by a complex interplay between physiological pathways, biochemical processes, and physical mechanisms. This study aimed to develop an in-silico physics-based approach to comprehensively model the multifaceted vascular pathophysiological adaptations. This approach focused on capturing the progression of proximal pulmonary arterial hypertension, which is significantly associated with the irreversible degradation of arterial walls and compensatory stress-induced growth and remodeling. This study incorporated critical characteristics related to the distinct time scales for the deformation, thus reflecting the impact of mean pressure on artery growth and tissue damage. The in-silico simulation of the progression of pulmonary hypertension was realized based on computational code combined with the finite element method (FEM) for the simulation of disease progression. The parametric studies further explored the consequences of these irreversible processes. This computational modeling approach may advance our understanding of pulmonary hypertension and its progression.

Phylogenomic curation of Ovate Family Proteins (OFPs) in the U's Triangle of Brassica L. indicates stress-induced growth modulation.

The Ovate Family Proteins (OFPs) gene family houses a class of proteins that are involved in regulating plant growth and development. To date, there is no report of the simultaneous functional characterization of this gene family in all members of U's Triangle of Brassica. Here, we retrieved a combined total of 256 OFP protein sequences and analyzed their chromosomal localization, gene structure, conserved protein motif domains, and the pattern of cis-acting regulatory elements. The abundance of light-responsive elements like G-box, MRE, and GT1 motif suggests that OFPs are sensitive to the stimuli of light. The protein-protein interaction network analysis revealed that OFP05 and its orthologous genes were involved in regulating the process of transcriptional repression through their interaction with homeodomain transcription factors like KNAT and BLH. The presence of domains like DNA binding 2 and its superfamily speculated the involvement of OFPs in regulating gene expression. The biotic and abiotic stress, and the tissue-specific expression analysis of the RNA-seq datasets revealed that some of the genes such as BjuOFP30, and BnaOFP27, BolOFP11, and BolOFP10 were highly upregulated in seed coat at the mature stage and roots under various chemical stress conditions respectively which suggests their crucial role in plant growth and development processes. Experimental validation of prominent BnaOFPs such as BnaOFP27 confirmed their involvement in regulating gene expression under salinity, heavy metal, drought, heat, and cold stress. The GO and KEGG pathway enrichment analysis also sheds light on the involvement of OFPs in regulating plant growth and development. These findings have the potential to serve as a forerunner for future studies in terms of functionally diverse analysis of the OFP gene family in Brassica and other plant species.

Tim-3 deficiency aggravates cadmium nephrotoxicity via regulation of NF-κB signaling and mitochondrial damage

Kidney is the target organ of serious cadmium injury. Kidney damage caused by cadmium exposure is greatly influenced by the inflammatory response and mitochondrial damage. T cell immunoglobulin domain and mucin domain 3 (Tim-3) is an essential protein that functions as a negative immunological checkpoint to regulate inflammatory responses. Mice were given cadmium treatments at various dosages (0, 1.5, 3, 4.5 mg/kg) and times (0, 3, 5, 7 days) to assess the effects of cadmium on kidney damage. We found that the optimal way to induce kidney injury in mice was to inject 4.5 mg/kg of cadmium intraperitoneally for five days. It is interesting that giving mice 4.5 mg/kg of cadmium intravenously for seven days drastically lowered their survival rate. After cadmium exposure, Tim-3 knockout mice exhibited higher blood concentrations of urea nitrogen and creatinine compared to control mice. Tim-3 impacted the expression of oxidative stress-associated genes such as UDP glucuronosyltransferase family 1 member A9 (Ugt1a9), oxidative stress-induced growth inhibitor 2 (Osgin2), and S100 calcium binding protein A8 (S100a8), according to RNA-seq and real-time RT-PCR data. Tim-3 deficiency also resulted in activated nuclear factor-kappa B (NF-κB) signaling pathway. The NF-κB inhibitor 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1) significantly alleviated cell apoptosis, oxidative stress response, and renal tubule inflammation in Tim-3 knockout mice exposed to cadmium. Furthermore, cadmium caused obvious B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax) translocation from cytoplasm to mitochondria, which can be inhibited by TPCA-1. In conclusion, Tim-3 prevented mitochondrial damage and NF-κB signaling activation, hence providing protection against cadmium nephrotoxicity.

Extracellular pectin-RALF phase separation mediates FERONIA global signaling function

The FERONIA (FER)-LLG1 co-receptor and its peptide ligand RALF regulate myriad processes for plant growth and survival. Focusing on signal-induced cell surface responses, we discovered that intrinsically disordered RALF triggers clustering and endocytosis of its cognate receptors and FER- and LLG1-dependent endocytosis of non-cognate regulators of diverse processes, thus capable of broadly impacting downstream responses. RALF, however, remains extracellular. We demonstrate that RALF binds the cell wall polysaccharide pectin. They phase separate and recruit FER and LLG1 into pectin-RALF-FER-LLG1 condensates to initiate RALF-triggered cell surface responses. We show further that two frequently encountered environmental challenges, elevated salt and temperature, trigger RALF-pectin phase separation, promiscuous receptor clustering and massive endocytosis, and that this process is crucial for recovery from stress-induced growth attenuation. Our results support that RALF-pectin phase separation mediates an exoskeletal mechanism to broadly activate FER-LLG1-dependent cell surface responses to mediate the global role of FER in plant growth and survival.

Characterization of a Novel Polysaccharide Derived from Rhizospheric Paecilomyces vaniformisi and Its Mechanism for Enhancing Salinity Resistance in Rice Seedlings.

Soil salinity is an important limiting factor in agricultural production. Rhizospheric fungi can potentially enhance crop salinity tolerance, but the precise role of signaling substances is still to be systematically elucidated. A rhizospheric fungus identified as Paecilomyces vaniformisi was found to enhance the salinity tolerance of rice seedlings. In this study, a novel polysaccharide (PPL2b) was isolated from P. vaniformisi and identified as consisting of Manp, Glcp, GalpA, and Galp. In a further study, PPL2b showed significant activity in alleviating salinity stress-induced growth inhibition in rice seedlings. The results indicated that under salinity stress, PPL2b enhances seed germination, plant growth (height and biomass), and biochemical parameters (soluble sugar and protein contents). Additionally, PPL2b regulates genes such as SOS1 and SKOR to decrease K+ efflux and increase Na+ efflux. PPL2b increased the expression and activity of genes related to antioxidant enzymes and nonenzyme substances in salinity-induced oxidative stress. Further study indicated that PPL2b plays a crucial role in regulating osmotic substances, such as proline and betaine, in maintaining the osmotic balance. It also modulates plant hormones to promote rice seedling growth and enhance their tolerance to soil salinity. The variables interacted and were divided into two groups (PC1 77.39% and PC2 18.77%) based on their relative values. Therefore, these findings indicate that PPL2b from P. vaniformisi can alleviate the inhibitory effects of salinity stress on root development, osmotic adjustment, ion balance, oxidative stress balance, and growth of rice seedlings. Furthermore, it suggests that polysaccharides produced by rhizospheric fungi could be utilized to enhance crop tolerance to salinity.

Heat Stress-Induced Fetal Intrauterine Growth Restriction Is Associated with Elevated LPS Levels Along the Maternal Intestine-Placenta-Fetus Axis in Pregnant Mice.

The exacerbation of the greenhouse effect has made heat stress (HS) an important risk factor for the occurrence of intrauterine growth restriction (IUGR). The experiment aims to uncover the effects of maternal HS on IUGR and its mechanisms. The results showed that HS leads to decreased maternal and fetal birth weights, accompanied by increased serum oxidative stress and cortisol levels. Moreover, HS inflicted significant damage to both the intestinal and placental barriers, altering maternal gut microbiota and increasing intestinal LPS levels. As a result, LPS levels increased in maternal serum, placenta, and fetus. Furthermore, HS damaged the intestinal structure, intensifying inflammation and disrupting the redox balance. The placenta exposed to HS exhibited changes in the placental structure along with disrupted angiogenesis and decreased levels of nutritional transporters. Additionally, the leakage of LPS triggered placental JNK and ERK phosphorylation, ultimately inducing severe placental inflammation and oxidative stress. This study suggests that LPS translocation from the maternal intestine to the fetus, due to a disrupted gut microbiota balance and compromised intestinal and placental barrier integrity, may be the primary cause of HS-induced IUGR. Furthermore, increased LPS leakage leads to placental inflammation, redox imbalance, and impaired nutrient transport, further restricting fetal growth.

Numerical investigation of the mechano-electro-chemical effect of X100 buried pipelines with pre-existing corrosion defects

This study investigates the corrosion kinetics and crack propagation in buried transmission pipelines made of high-strength low alloy steel API X100. Despite its cost-effectiveness and ability to withstand high operating conditions without increasing pipe wall thickness, the corrosion kinetics in near-neutral pH environments for this steel grade is not fully understood. To address this gap, two numerical models were developed. The first model, using COMSOL Multiphysics v5.6, showed higher electrolyte potential at the corrosion defect center due to stress-induced defect growth, increasing corrosion susceptibility. The second model, employing the XFEM approach, evaluated crack initiation, propagation, and von Mises stress distribution along the crack path. This research contributes to a better understanding of corrosion and crack behavior in corroded pipelines, aiding in their performance improvement in near-neutral pH soil environments.

442 Awardee Talk: Adaptive Programming of Poor Skeletal Muscle Growth and Metabolism Associated with Heat Stress-Induced Intrauterine Growth Restriction

Abstract Intrauterine growth restriction (IUGR) is associated with reduced β2 adrenergic sensitivity, which contributes to poor postnatal muscle growth and metabolic inefficiency. Thus, our objective was to determine if stimulating β2 adrenergic activity would rescue deficits in muscle growth, body composition, and indicators of metabolic homeostasis in IUGR offspring. Maternal heat stress (40°C, 35% humidity, THI = 85) from d 40 to 95 of gestation was used to produce IUGR lambs. From birth, IUGR lambs received daily IM injections of saline (IUGR; n = 12) or 0.8 μg/kg clenbuterol HCl (IUGR+CLEN; n = 11). Placebo-injected controls (n = 13) were born to pair-fed thermoneutral ewes. Body composition was estimated by ultrasound and bioelectrical impedance analyses (BIA) at d 58. Lambs were catheterized at d 55 and necropsied at d 60. Square-wave hyperglycemic clamps and indirect calorimetry were performed at d 57. Hyperinsulinemic-euglycemic clamps were performed at d 58. Bodyweights were lighter (P ≤ 0.05) for IUGR and IUGR+CLEN lambs than for controls at birth, d 30, and d 60. Average daily gain was less (P ≤ 0.05) for IUGR compared with controls and was intermediate for IUGR+CLEN lambs. BIA-estimated fat-free mass, ultrasound-estimated loin eye area (LEA), actual LEA, and flexor digitorum superficialis (FDS) muscle weight were less (P ≤ 0.05) for IUGR but not IUGR+CLEN lambs than for controls. Semitendinosus from IUGR lambs had less (P ≤ 0.05) β2 adrenoreceptor content, fewer (P ≤ 0.05) proliferating myoblasts, tended to have fewer (P = 0.08) differentiated myoblasts, and had smaller (P ≤ 0.05) muscle fibers than controls. Proliferating myoblasts and fiber size but not β2 adrenoreceptor content or differentiated myoblasts were rescued (P ≤ 0.05) in IUGR+CLEN lambs compared with IUGR lambs. Basal plasma insulin did not differ, but glucose-stimulated insulin secretion was 44% less (P ≤ 0.05) for IUGR lambs than for controls and was intermediate for IUGR+CLEN lambs. Basal and insulin-stimulated hindlimb glucose uptake and basal glucose oxidation did not differ among groups. Insulin-stimulated glucose oxidation was 54% less (P ≤ 0.05) for IUGR lambs but not IUGR+CLEN lambs compared with controls. Ex vivo glucose uptake was 25% less (P ≤ 0.05) for FDS from IUGR and IUGR+CLEN lambs than from controls. Ex vivo glucose oxidation was less (P ≤ 0.05) for FDS and soleus from IUGR lambs compared with controls and was intermediate (P ≤ 0.05) for FDS but not soleus from IUGR+CLEN lambs. Whole-body O2 consumption was 22% less (P ≤ 0.05) for IUGR and IUGR+CLEN lambs than for controls. Whole-body CO2 production was 17% less (P ≤ 0.05) for IUGR but not IUGR+CLEN lambs than for controls. These findings show that IUGR muscle remained responsive to β2 adrenergic stimulation despite reduced β2 adrenoreceptor content, and thus β2 adrenergic pathways may be a strategic target for improving muscle growth, body composition, and metabolic efficiency in IUGR-born offspring.

CGMP functions as an important messenger involved in SlSAMS1-regulated salt stress tolerance in tomato

Salt stress adversely affects the growth, development, and yield of tomato (Solanum lycopersicum). SAM Synthetase (SAMS), which is responsible for the biosynthesis of S-adenosylmethionine (SAM, a precursor of polyamine biosynthesis), participates in plant response to abiotic stress. However, the regulatory mechanism of SAMS-mediated salt stress tolerance remains elusive. In this study, we characterized a SAMS homologue SlSAMS1 in tomato. We found that SlSAMS1 is highly expressed in tomato roots, and its expression can be induced by salt stress. Crucially, overexpression of SlSAMS1 in tomato enhances salt stress tolerance. Through metabolomic profiling, we identified some differentially accumulated metabolites, especially, a secondary messenger guanosine 3′,5′-cyclic monophosphate (cGMP) which may play a key role in SlSAMS1-regulated salt tolerance. A series of physiological and biochemical data suggest that cGMP alleviates salt stress-induced growth inhibition, and potentially acts downstream of the polyamine-nitric oxide (PA-NO) signaling pathway to trigger H2O2 signaling in response to salt stress. Taken together, the study reveals that SlSAMS1 regulates tomato salt tolerance via the PA–NO–cGMP-H2O2 signal module. Our findings elucidate the regulatory pathway of SlSAMS1-induced plant response to salt stress and indicate a pivotal role of cGMP in salt tolerance.