Mei Yu

Avian Pathogenic Escherichia coli (APEC) is a major causative agent of colibacillosis, a severe respiratory disease in birds that leads to significant economic losses in poultry production industry. The two-component systems (TCSs) CitA/CitB regulates metabolism and stress adaptation in Enterobacteriaceae, but its contribution to virulence, particularly in APEC, is undefined. In this study, we investigated the function of the CitA/CitB in APEC by analyzing the transcriptional profile of wild-type strain APEC40 compared to a citAB-deletion mutant. Microarray analysis revealed that CitA/CitB significantly impacts the transcription of numerous genes, including multiple genes associated with biofilm formation and virulence. Phenotypic assays confirmed that inactivation of citAB significantly enhanced biofilm formation capacity and multidrug resistance. Quantitative real-time PCR (qRT-PCR) analysis demonstrated that CitAB negatively regulates expression of key genes involved in these phenotypes, including mglB, fimB, glcB, mblC, ompC, ompW, and pgaB. Collectively, these results demonstrate that the CitA/CitB acts as a negative regulator of biofilm formation, multidrug resistance, and key virulence-associated genes in APEC.

Nitric oxide (NO) has been firmly established as a key signaling molecule in plants, playing a significant role in regulating growth, development and stress responses. Given the imperative of sustainable agriculture and the urgent need to meet the escalating global demand for food, it is imperative to safeguard crop plants from the effects of climate fluctuations. Plants respond to environmental challenges by producing redox molecules, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), which regulate cellular, physiological, and molecular processes. Nitric oxide (NO) plays a crucial role in plant stress tolerance, acting as a signaling molecule or free radical. NO is involved in various developmental processes in plants through diverse mechanisms. Exogenous NO supplementation can alleviate the toxicity of abiotic stresses and enhance plant resistance. In this review we summarize the studies regarding the production of NO in peroxisomes, and how its molecule and its derived products, (ONOO⁻) and S-nitrosoglutathione (GSNO) affect ROS metabolism in peroxisomes. Peroxisomal antioxidant enzymes including catalase (CAT), are key targets of NO-mediated post-translational modification (PTM) highlighting the dynamic metabolism of ROS and RNS in peroxisomes.

Micronuclei (MNi) are extensively used to evaluate genotoxic effects and chromosome instability. However, the roles of kinetochore of MN in mitosis have not been completely addressed. The HeLa CENP B-GFP H2B-mCherry cells are applied to address these questions via the long-term live-cell imaging. In the cells, the kinetochore-positive micronucleus (K+MN) contained CENP B-GFP, while the kinetochore-negative micronucleus (K−MN) did not. K−MN-bearing cells produced much more chromosome fragments than did MN-free cells. Most of the chromosome fragments eventually merged into K−MNi. K+MN-bearing cells yielded more kinetochore-positive lagging chromosomes (K+LCs) and K+MNi than MN-free cells did. The results suggested the differences in the fates of K+MNi and K−MNi in mitosis. The cycle of K−MN → Chromosome fragment → K−MN may occur in generations of K−MN-bearing cells, while part of K+MNi might reincorporate into the main nucleus. The K+MN-bearing cells prolonged significantly duration of mitosis compared with MN-free cells. The presence of micronuclei, regardless of K−MN and K+MN, enhanced apoptosis cell death. And K+MN-bearing cells were inclined to apoptosis more than K−MN-bearing cells. The results suggested differences in fates between K−MN-bearing and K+MN-bearing cells. Kinetochore determined the fates of micronuclei. Kinetochore in micronuclei indirectly prolonged the duration of mitosis. Kinetochore enhanced cytotoxicity of micronuclei. Our data are direct evidences showing the roles of kinetochore of micronucleus in mitosis of HeLa cells.