Mobile DNA最新文献

Genome size expansions are common among eukaryotic lineages. Enlarged genomes can be bioenergetically demanding, and active mobile elements can trigger chromosomal rearrangements and loss of gene function. What triggers genome size expansions remains largely unexplored in many biological clades, particularly within the fungal kingdom. Activation of large transposable elements (TEs), such as long-terminal repeats (LTRs), is a common contributor. Yet the mechanisms of LTR activation remain poorly understood. Here, we focus on the fungal genus Pseudocercospora and closely related species with known variation in genome size. In using an assembly-free approach, we found that TE content is highly variable among species, with species-specific retrotransposon families being the main drivers of independent genome expansions. We further focused on the two species with the most expanded genomes and reference-quality genomes, P. fijiensis and P. ulei. We found that the P. ulei genome is compartmentalized, with highly variable TE densities among chromosomal regions, and a striking reduction in pathogenicity-associated genes. Overall, our study indicates that species of Pseudocercospora originally had reduced genome sizes, and genome expansions are species-specific, driven by heterogeneous sets of TE families. We discuss what might have caused TE activation and subsequent proliferation in the genus, including stress conditions and host adaptation. Surveys of clades with highly dynamic genome sizes are crucial for the investigation of causal factors driving long-term TE dynamics.

The seventh Japanese meeting on host-transposon interactions, titled "Biological Function and Evolution through Interactions between Hosts and Transposable Elements," was held on September 1st and 2nd, 2025, at the National Institute of Genetics, as well as online. This meeting was supported by the National Institute of Genetics and aimed to bring together researchers studying the diverse roles of transposable elements (TEs) in genome function and evolution, as well as host defense systems against TE mobility, TE bursts during evolution, and intron mobility in mammals, insects, land plants, fungi, and protozoa. Here, we present the highlights of these discussions.

How endogenous retroviral elements (ERVs), a family of transposable elements, may promote tumor progression is not well understood. Tripartite motif-containing 28 (TRIM28/TIF1b/KAP1) is a key transcriptional co-repressor protein that represses ERV expression in many cell types including embryonic stem cells, neural progenitor cells, differentiated adult cells, and cancer cells. In this study, we investigated the effect of Trim28 deletion on the expression of ERVs using an immune competent genetically engineered mouse model for prostate cancer. We found Trim28 deletion in prostate tumors led to the expression of ERVs in prostates from both hormonally intact and castrated mice. ERVs can regulate the expression of neighboring genes, and we detected increased expression of several protein-coding genes near overexpressed ERVs. Our data suggest that Trim28 deletion in prostate tumor epithelial cells may promote an innate immune response. However, Trim28 deletion also led to excessive deposition of tumor extracellular matrix (ECM). Our findings suggest that ECM alterations downstream of ERV derepression could affect immune cells in the tumor microenvironment and may promote tumor progression.