Abstract Fusarium wilt of banana is a destructive soilborne fungal disease that threatens global production. The disease is caused by different physiological races of Fusarium oxysporum f. sp. cubense (Foc). Using PacBio HiFi sequencing, we assembled and annotated the complete mitochondrial genomes of two Brazilian isolates representing race 1 (R1; strain 0801) and subtropical race 4 (STR4; strain 218A) to clarify phylogenetic relationships among Foc races and identify genetic variation suitable for diagnostic development. Both mitogenomes contained a conserved core region and a long variable region (LVR). The 51,473 bp R1 mitogenome comprised 15 protein-coding genes, 2 rRNA genes, 30 tRNA genes, and an LVR corresponding to LVR2 described in F. oxysporum. The 49,948 bp STR4 mitogenome included the same set of protein-coding and rRNA genes, 26 tRNA genes, and an LVR1. Phylogenetic analysis revealed a clear separation between R1 and R4 lineages, while also reflecting a closer mitochondrial relationship of STR4 to TR4. These findings are consistent with previous evidence of mitochondrial exchange within the F. oxysporum complex and underscore the importance of expanded mitogenome sampling across Foc races to refine phylogenetic frameworks and to identify robust, race-informative mitochondrial markers for sensitive and specific molecular diagnostics.
Abstract Mitochondria are essential organelles in mammalian cells, performing multiple functions ranging from energy metabolism and intracellular signaling to the regulation of cell fate. Proper mitochondrial function depends on the coordinated expression of two distinct genomes: the nuclear genome and the mitochondrial genome, known as mitochondrial DNA (mtDNA). Although most mitochondrial proteins are encoded by nuclear genes, mtDNA encodes 13 polypeptides that are essential components of the oxidative phosphorylation (OXPHOS) system and ATP production. For reasons that are not yet fully understood, mtDNA accumulates DNA damage at levels estimated to be 1-5 times higher than those observed in nuclear DNA, underscoring the importance of efficient DNA repair and damage tolerance mechanisms within mitochondria. Mammalian mitochondria are competent in several DNA repair pathways, with base excision repair being the best characterized. However, the molecular mechanisms underlying DNA damage response (DDR) pathways activated by mtDNA lesions remain poorly defined. In this review, we briefly summarize the established DNA repair pathways operating in mammalian mitochondria, which have been extensively discussed elsewhere, and focus primarily on DDR components implicated in the response to mtDNA damage, as well as on the cellular consequences of mtDNA damage accumulation.
Abstract DNA crosslinks are cytotoxic lesions caused by a variety of DNA reacting compounds. Some bacterial competitors and environmental organisms evolved the ability to synthesize and secrete alkylating molecules that bind to DNA, impairing replication and transcription and ultimately resulting in death of the target cells. Notwithstanding, environmental exposure, spontaneous chemical reactions and byproducts of the physiological metabolism can interfere with DNA, leading to toxic crosslinking damage. Hence, bacteria evolved repair systems capable of removing lesions and allowing cells to thrive even in harsh conditions. Base Excision Repair, Nucleotide Excision Repair, Homologous Recombination and Translesion Synthesis all combine to solve DNA monoadducts, Intrastrand, Interstrand, and DNA-Peptide Crosslinks. In this review, we address major stressors to which bacteria are exposed, their DNA-damaging capacities and how the prokaryotic cell responds.
Abstract Plant-microorganism interactions contribute to plant health by enhancing nutrient acquisition. The transcription factor OsASR5 regulates detoxification gene expression under aluminum stress in rice and is implicated as a positive regulator of responses to iron and phosphorus deficiency. Given its role in nutrient regulation, we investigated whether OsASR5 influences the assembly of the rice microbiome. In this study, we characterized the bacteria communities associated with the leaves and roots of OsASR5-RNAi rice plants compared to wild-type Oryza sativa cv. Nipponbare. Notably, OsASR5-RNAi plants showed altered bacterial beta diversity compared with wild type. The bacterial composition of OsASR5-RNAi plants differed in both organs, with decreased Desulfobacteriota and increased in Acidobacteria abundance in leaves. At the genus level, Methylobacterium, a known plant growth promoter, was less prevalent in leaves, while Magnetospirillum, associated with iron cycling, was less abundant in roots. Conversely, several bacteria were more abundant in OsASR5-RNAi plants, including Aneurinibacillus, Anaeromyxobacter, and Methylobacter, which are associated with nitrogen cycling and phosphorus solubilization. Additionally, Geobacter and Geothrix, both known for their role in metal reduction, particularly iron, were more abundant in OsASR5-RNAi plants. These suggest that OsASR5 affects plant-microbe interactions, potentially influencing nutrient cycling and plant stress responses through microbiome modulation.
Abstract 1α,25-(OH)2-D3 can promote autophagy of osteoclast precursors (OCPs), resulting in its pro-osteoclastogenic effect, which limits its anti-osteoporotic efficacy. To address the above challenges, we need to explore the targets of autophagy-enhancing effect of 1α,25-(OH)2-D3. These results showed that 1α,25-(OH)2-D3 promoted the expression of BECN1 mRNA and Beclin1 protein in OCPs under RANKL induction. Furthermore, 1α,25-(OH)2-D3 enhances p65 phosphorylation and nuclear translocation. The lentiviral-mediated silencing of both BECN1 and p65 impeded the facilitation of 1α,25-(OH)2-D3 on osteoclast differentiation and OCP autophagy. Moreover, p65 silencing blocked the enhancement of BECN1 mRNA expression and Beclin1 protein expression by 1α,25-(OH)2-D3. In conclusion, 1α,25-(OH)2-D3 enhances Beclin1-dependent autophagy in OCPs by promoting BECN1 transcription, thereby promoting osteoclast differentiation; this indicates that the therapeutic strategies for BECN1 or p65 targeted inhibition have the potential to optimize the anti-osteoporotic function of 1α,25-(OH)2-D3.
