98%
921
2 minutes
20
Hyperosmolality-triggered physiological drought hinders plant growth and development, leading to a drop in crop yields. Hyperosmolality triggers calcium signaling, and yet how osmotic-induced calcium signaling participates in cellular osmotic response remains enigmatic. To date, several Ca channels and transporters have been identified to regulate osmotic-induced calcium signal generation (CaSG) or Ca homeostasis. However, there has been no report on their function in calcium signal clearance (CaSC) in plants, especially in crops. Here, we investigated the role of a rice cation/calcium exchanger OsCCX2 in modulating calcium signaling dynamics using two distinct calcium reporters aequorin and GCaMP6s. The results showed that, under osmotic stress conditions, CaSC was significantly delayed in both root and guard cells of ccx2 mutants compared with the wild-type. Further studies revealed that hyperosmotic stress-triggered influxes of sodium (Na), potassium (K), and chloride (Cl) ions were significantly reduced in ccx2 mutants, resulting in a significantly smaller range of osmotic pressure and water potentials (Ψ) adjustment. In addition, the stomatal response was impaired, with a faster water loss in ccx2 in response to hyperosmotic stress. Furthermore, the absence of OsCCX2 altered the expression patterns of key osmotic-responsive genes, but their transcriptional activation was unaffected. Collectively, these changes ultimately led to reduced hyperosmotic stress tolerance in the mutants. Additionally, OsCCX2 is likely to be located in the endoplasmic reticulum and plasma membrane, and possess Na/Ca exchange activity. To sum up, our findings provide evidence that OsCCX2, as a CaSC regulator, is involved in cell osmotic adjustment, water homeostasis and osmotic stress tolerance in rice, which offers new insight into potential applications in drought-resistant crop improvement.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/jipb.70029 | DOI Listing |
Proc Natl Acad Sci U S A
September 2025
Department of Neuroscience, The Scripps Research Institute, San Diego, CA 92037.
Microglia regulate neuronal circuit plasticity. Disrupting their homeostatic function has detrimental effects on neuronal circuit health. Neuroinflammation contributes to the onset and progression of neurodegenerative diseases, including Alzheimer's disease (AD), with several microglial activation genes linked to increased risk for these conditions.
View Article and Find Full Text PDFJ Vis Exp
August 2025
Laboratory of Regenerative Medicine in Sports Science, School of Physical Education and Sports Science, South China Normal University; Bone and Joint Research Team of Degeneration and Injury, Guangdong Provincial Academy of Chinese Medical Sciences;
Post-traumatic osteoarthritis (PTOA) is a degenerative joint disease triggered by trauma or intense mechanical stress, leading to joint cartilage degeneration and functional impairment. Prostaglandin E2 (PGE2) contributes significantly to cartilage degradation following mechanical injury by activating its receptor, Prostaglandin E receptor 4 (EP4), on chondrocyte membranes. The homeostasis of articular cartilage primarily relies on the dynamic balance between cartilage degradation and repair, a process finely regulated by chondrocytes.
View Article and Find Full Text PDFJ Vis Exp
August 2025
Department of Cardiology, First Hospital of Nanping City affiliated to Fujian Medical University;
Myocardial ischemia-reperfusion injury (MIRI) endures as a substantial impediment to the management of cardiovascular disease. The pathophysiology of MIRI is complex, involving oxidative stress, calcium overload, inflammation, and apoptosis. The NRG1/ErbB4 signaling pathway has been implicated in modulating oxidative stress responses in the heart, potentially reducing cellular damage caused by free radicals.
View Article and Find Full Text PDFElife
September 2025
Department of Chemistry, University of Massachusetts, Amherst, United States.
Voltage-dependence gating of ion channels underlies numerous physiological and pathophysiological processes, and disruption of normal voltage gating is the cause of many channelopathies. Here, long timescale atomistic simulations were performed to directly probe voltage-induced gating transitions of the big potassium (BK) channels, where the voltage sensor domain (VSD) movement has been suggested to be distinct from that of canonical Kv channels but remains poorly understood. Using a Core-MT construct without the gating ring, multiple voltage activation transitions were observed at 750 mV, allowing detailed analysis of the activated state of BK VSD and key mechanistic features.
View Article and Find Full Text PDFRegen Med
September 2025
Symbiosis Centre for Stem Cell Research (SCSCR), Symbiosis School of Biological Sciences (SSBS), Symbiosis International, Deemed University, Lavale, Pune, India.
Aims: This study aimed to enhance the osteoinductive potential of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) by integrating them into a nano-hydroxyapatite (nHAp)-enriched hydrogel scaffold for bone regeneration applications.
Materials & Methods: EVs were isolated from naïve and osteogenically primed MSCs and characterized for morphology, cargo content, and cytocompatibility. Their uptake and osteoinductive activity were assessed using MC3T3 cells within a 3D interpenetrating network (IPN) hydrogel.