We applied the RFLP approach to identify the cytoplasmic genotypes of selected onion breeding materials from Poland. For this purpose, mitochondrial DNA from cytoplasmic male-sterile (CMS) and male-fertile onions were hybridized with the probes for the following mitochondrial genes: atpA, atp6, atp9, cob, cox1, nad3, nad4 and nad6. S-, T- or C-cytoplasm was represented in each analyzed sterile accession. Some new polymorphisms shared by S- and C-cytoplasmic onions were identified. We also used currently available PCR markers to test if cytoplasmic heterogenity occurs within onion inbreds. A fraction of the plants bearing S-cytoplasm were found within two male-fertile lines, but such plants were not detected in the open-pollinated cultivars Sochaczewska, Wolska and Zytawska. Both the RFLP and PCR approaches gave some proof of existing mitochondrial heteroplasmy in onions
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BMC Nephrol
January 2025
Department of Nephrology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Background: Infectious episodes contribute to morbidity and mortality in patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Renal involvement, also known as ANCA-associated glomerulonephritis (AGN), is frequently observed in AAV. Little is known about whether co-infection at initial diagnosis is associated with renal outcome and prognosis in children with AGN.
View Article and Find Full Text PDFNat Neurosci
January 2025
Department of Neurobiology & Behavior, University of California, Irvine, Irvine, CA, USA.
Huntington's disease (HD) is caused by a CAG repeat expansion in the HTT gene, leading to altered gene expression. However, the mechanisms leading to disrupted RNA processing in HD remain unclear. Here we identify TDP-43 and the N6-methyladenosine (m6A) writer protein METTL3 to be upstream regulators of exon skipping in multiple HD systems.
View Article and Find Full Text PDFInflamm Res
January 2025
Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, The First Dongguan Affiliated Hospital, College of Medical Technology, Guangdong Medical University, Dongguan, 523808, China.
Allergic asthma is a chronic complex airway disease characterized by airway hyperresponsiveness, eosinophilic inflammation, excessive mucus secretion, and airway remodeling, with increasing mortality and incidence globally. The pathogenesis of allergic asthma is influenced by various factors including genetics, environment, and immune responses, making it complex and diverse. Recent studies have found that various cellular functions of mitochondria such as calcium regulation, adenosine triphosphate production, changes in redox potential, and free radical scavenging, are involved in regulating the pathogenesis of asthma.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Division of Experimental Chemotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo, Japan.
KRAS-specific inhibitors have shown promising antitumor effects, especially in non-small cell lung cancer, but limited efficacy in colorectal cancer (CRC) patients. Recent studies have shown that EGFR-mediated adaptive feedback mediates primary resistance to KRAS inhibitors, but the other resistance mechanisms have not been identified. In this study, we investigated intrinsic resistance mechanisms to KRAS inhibitors using patient-derived CRC cells (CRC-PDCs).
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopedic Surgery at the First Affiliated Hospital, Harbin Medical University, Harbin, China.
Osteoporosis (OP) is a prevalent age-related bone metabolic disease. Aging and mitochondrial dysfunction are involved in the onset and progression of OP, but the specific mechanisms have not been elucidated. The aim of this study was to identify novel potential biomarkers associated with aging and mitochondria in OP.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!