98%
921
2 minutes
20
Water scarcity and corresponding abiotic drought stress is one of the most important factors limiting plant performance and yield. In addition, plant productivity is severely compromised worldwide by infection with microbial pathogens. Two of the most prominent pathways responsible for drought tolerance and disease resistance to fungal pathogens in Arabidopsis are those controlled by the phytohormones abscisic acid (ABA) and the oxylipin methyl jasmonate (MeJA), respectively. Here, we report on the functional characterization of OCP3, a transcriptional regulator from the homeodomain (HD) family. The Arabidopsis loss-of-function ocp3 mutant exhibits both drought resistance and enhanced disease resistance to necrotrophic fungal pathogens. Double-mutant analysis revealed that these two resistance phenotypes have different genetic requirements. Whereas drought tolerance in ocp3 is ABA-dependent but MeJA-independent, the opposite holds true for the enhanced disease resistance characteristics. These observations lead us to propose a regulatory role of OCP3 in the adaptive responses to these two stresses, functioning as a modulator of independent and specific aspects of the ABA- and MeJA-mediated signal transduction pathways.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/j.1365-313X.2009.03804.x | DOI Listing |
Zhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
School of Sports Medicine and Rehabilitation, Beijing Sport University, Beijing 100084, China.
Multimorbidity of chronic diseases is one of the most common health issues among older adults, and the resulting demand for long-term medical care and management imposes a considerable burden on healthcare systems. Muscle strength, a core indicator of overall health status, is closely associated with the risk of developing multimorbidity of chronic diseases in older adults. Decline in muscle strength not only increases the risk of multimorbidity of chronic diseases but also interacts with it to exacerbate disease burden.
View Article and Find Full Text PDFChem Biol Drug Des
September 2025
Laboratory of Biochemistry and Animal Toxins, Institute of Biotechnology, Federal University of Uberlandia, Uberlandia, MG, Brazil.
Leishmaniasis, a disease caused by Leishmania parasites, poses a significant health threat globally, particularly in Latin America and Brazil. Leishmania amazonensis is an important species because it is associated with both cutaneous leishmaniasis and an atypical visceral form. Current treatments are hindered by toxicity, resistance, and high cost, driving the need for new therapeutic targets and drugs.
View Article and Find Full Text PDFEur J Heart Fail
September 2025
Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Aims: The estimated glucose disposal rate (eGDR) is a simple, non-invasive measure of insulin resistance. In this exploratory analysis of FINEARTS-HF, we evaluated whether lower eGDR, reflecting greater insulin resistance, is associated with adverse outcomes in heart failure (HF).
Methods And Results: The eGDR was calculated at baseline using waist circumference, glycated haemoglobin, and hypertension status.
Protein Cell
September 2025
Department of Human Cell Biology and Genetics, SUSTech Homeostatic Medicine Institute, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Breast cancer is a prevalent malignancy worldwide. The majority of breast cancers belong to the estrogen receptor (ER)-positive luminal subtype that can be effectively treated with antiestrogen therapies. However, a significant portion of such malignancies become hormone-refractory and incurable.
View Article and Find Full Text PDFBMB Rep
September 2025
Basic Research Laboratory, Department of Physiology, College of Medicine, Smart Marine Therapeutic Center, Cardiovascular and Metabolic Disease Core Research Center, Inje University, Busan 47392, Korea; Department of Health Science and Technology, College of Medicine, Inje University, Busan 47392, K
Patients with multiple myeloma develop resistance to thalidomide during therapy, and the mechanisms to counteract thalidomide resistance remain elusive. Here, we explored the interaction between cereblon and mitochondrial function to mitigate thalidomide resistance in multiple myeloma. Measurements of cell viability, ATP production, mitochondrial membrane potential, mitochondrial ROS, and protein expression via western blotting were conducted in vitro using KSM20 and KMS26 cells to assess the impact of thalidomide on multiple myeloma.
View Article and Find Full Text PDF