Post-polyploidization centromere evolution in cotton
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Polyploidization plays an important role in plant speciation and adaptation. To address the role of polyploidization in grass diversification, we studied Phragmites australis, an invasive species with intraspecific variation in chromosome numbers ranging from 2n = 36 to 144. We utilized a combined analysis of ploidy estimation, phylogeny, population genetics and model simulations to investigate the evolution of P. australis. Using restriction site-associated DNA sequencing (RAD-seq), we conducted a genome-wide analysis of 88 individuals sourced from diverse populations worldwide, revealing the presence of six distinct intraspecific lineages with extensive genetic admixture. Each lineage was characterized by a specific ploidy level, predominantly tetraploid or octoploid, indicative of multiple independent polyploidization events. The population size of each lineage has declined moderately in history while remaining large, except for the North American native and the US Land types, which experienced constant population size contraction throughout their history. Our investigation did not identify direct association between polyploidization events and grass invasions. Nonetheless, we observed octoploid and hexaploid lineages at contact zones in Romania, Hungary, and South Africa, suggestively due to genomic conflicts arising from allotetraploid parental lineages.
Microbiota transplantation for cotton leaf curl disease suppression—core microbiome and transcriptome dynamics
Microbiota transplantation is a strong tool for managing plant disease. This study investigates the effects of microbiota transplantation on Cotton Leaf Curl Disease (CLCuD) resistance in Gossypium hirsutum, a species with good fiber length but high susceptibility to biotic stresses. Using metabarcoding for V3-V4 16S rRNA gene amplicon, microbial fractions from both rhizosphere and phyllosphere of CLCuD-resistant species Gossypium arboreum, and susceptible cotton varieties are analyzed. Unique bacterial taxa have been identified associated with disease resistance. Interspecies and intraspecies microbiota transplantation is conducted, followed by CLCuD incidence assays. It is seen that rhizospheric microbiota transplantation from G. arboreum FDH228 significantly suppresses CLCuD in G. hirsutum varieties, outperforming exogenous salicylic acid application. While phyllospheric transplants also reduce disease incidence, they are less effective than rhizospheric transplants. Differential expression analysis DESeq2 is utilized to identify key bacterial genera correlated with CLCuD suppression, including Pseudoxanthomonas and Stenotrophomonas in the rhizosphere of G. arboreum FDH228. Functional pathway analysis reveals upregulation of stress response and metabolism in tolerant species. Transcriptomics reveals upregulation of genes involved in protein phosphorylation and stress response in interspecies rhizospheric microbiota transplants. This study highlights microbiota transplantation as a sustainable method for controlling CLCuD along with specific microbial and genetic mechanisms contributing to CLCuD resistance.
Unlocking the potential of experimental evolution to study drug resistance in pathogenic fungi
Exploring the dynamics and molecular mechanisms of antimicrobial drug resistance provides critical insights for developing effective strategies to combat it. This review highlights the potential of experimental evolution methods to study resistance in pathogenic fungi, drawing on insights from bacteriology and innovative approaches in mycology. We emphasize the versatility of experimental evolution in replicating clinical and environmental scenarios and propose that incorporating evolutionary modelling can enhance our understanding of antifungal resistance evolution. We advocate for a broader application of experimental evolution in medical mycology to improve our still limited understanding of drug resistance in fungi.
The cellular and molecular cardiac tissue responses in human inflammatory cardiomyopathies after SARS-CoV-2 infection and COVID-19 vaccination
Myocarditis, characterized by inflammatory cell infiltration, can have multiple etiologies, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or, rarely, mRNA-based coronavirus disease 2019 (COVID-19) vaccination. The underlying cellular and molecular mechanisms remain poorly understood. In this study, we performed single-nucleus RNA sequencing on left ventricular endomyocardial biopsies from patients with myocarditis unrelated to COVID-19 (Non-COVID-19), after SARS-CoV-2 infection (Post-COVID-19) and after COVID-19 vaccination (Post-Vaccination). We identified distinct cytokine expression patterns, with interferon-γ playing a key role in Post-COVID-19, and upregulated IL16 and IL18 expression serving as a hallmark of Post-Vaccination myocarditis. Although myeloid responses were similar across all groups, the Post-Vaccination group showed a higher proportion of CD4+ T cells, and the Post-COVID-19 group exhibited an expansion of cytotoxic CD8+ T and natural killer cells. Endothelial cells showed gene expression changes indicative of vascular barrier dysfunction in the Post-COVID-19 group and ongoing angiogenesis across all groups. These findings highlight shared and distinct mechanisms driving myocarditis in patients with and without a history of SARS-CoV-2 infection or vaccination.
Nasal anti-CD3 monoclonal antibody ameliorates traumatic brain injury, enhances microglial phagocytosis and reduces neuroinflammation via IL-10-dependent Treg–microglia crosstalk
Neuroinflammation plays a crucial role in traumatic brain injury (TBI), contributing to both damage and recovery, yet no effective therapy exists to mitigate central nervous system (CNS) injury and promote recovery after TBI. In the present study, we found that nasal administration of an anti-CD3 monoclonal antibody ameliorated CNS damage and behavioral deficits in a mouse model of contusional TBI. Nasal anti-CD3 induced a population of interleukin (IL)-10-producing regulatory T cells (Treg cells) that migrated to the brain and closely contacted microglia. Treg cells directly reduced chronic microglia inflammation and regulated their phagocytic function in an IL-10-dependent manner. Blocking the IL-10 receptor globally or specifically on microglia in vivo abrogated the beneficial effects of nasal anti-CD3. However, the adoptive transfer of IL-10-producing Treg cells to TBI-injured mice restored these beneficial effects by enhancing microglial phagocytic capacity and reducing microglia-induced neuroinflammation. These findings suggest that nasal anti-CD3 represents a promising new therapeutic approach for treating TBI and potentially other forms of acute brain injury.
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