Abstract:

A subset of human diseases originates from host genomic sequences, specifically through the involvement of transposons in chromosomal recombination and gene regulation. Transposons act as intrinsic modulators of genome architecture, functioning as remodelers and insertion vectors that may serve as regulatory DNA, functional RNA, or, in certain cases, proteins. Structural variability among transposons drives rapid increases in their abundance and contributes to genome expansion within relatively short evolutionary and adaptive timescales. These elements are highly conserved across distantly related taxonomic groups. Initially regarded as “junk DNA,” transposons are now understood to be fundamental elements of genomic construction, contributing to both structural organization and regulatory complexity. Furthermore, CRISPR-associated transposons represent promising molecular tools, enabling RNA-guided integration of large transgenes with significant potential for biotechnological applications.