Transposable elements (TEs) are mobile DNA sequences that can copy themselves throughout genomes, sometimes comprising >45% of mammalian genomes. Though mostly silenced, TEs contribute to evolution through insertional mutagenesis, recombination, and exaptation (co-option of TE sequences for new functions). TE activity varies across species and lineages.
From your study of DNA mutations, you know that changes to the genome — substitutions, insertions, deletions — provide the raw material for evolution. Transposable elements (TEs) represent an entirely different scale of genomic change: rather than single-nucleotide alterations, TEs are sequences hundreds to thousands of base pairs long that can move or copy themselves to new locations within the genome. They are sometimes called "jumping genes," a term coined by Barbara McClintock, who first discovered them in maize in the 1940s. Far from being rare curiosities, TEs make up roughly 45% of the human genome and over 80% of some plant genomes like maize.
TEs fall into two major classes based on their mechanism of movement. Class I elements (retrotransposons) use a "copy-and-paste" mechanism: they are transcribed into RNA, reverse-transcribed back into DNA, and the new DNA copy inserts at a new genomic location. The original copy stays put, so retrotransposons increase in copy number over time. LINEs (Long Interspersed Nuclear Elements) and SINEs (Short Interspersed Nuclear Elements, including the human Alu element) are the most abundant retrotransposons in mammalian genomes. Class II elements (DNA transposons) use a "cut-and-paste" mechanism: the element is excised from one location and inserted into another by a transposase enzyme. DNA transposons do not inherently increase in copy number, though replication timing can sometimes produce a net gain.
Most TE copies in any genome are inactive — mutated into silence over millions of years, or actively repressed by the host through DNA methylation and small RNA pathways. This is because TE insertions are usually neutral or harmful: an element landing inside a gene can disrupt its function, and ectopic recombination between dispersed TE copies can cause chromosomal rearrangements like deletions, duplications, and inversions. The genome and its TEs exist in a kind of evolutionary tension, with TEs "seeking" to replicate and the host genome evolving mechanisms to suppress them.
Yet TEs are far more than genomic parasites. Over evolutionary time, TE sequences have been exapted — co-opted for host functions — in remarkable ways. Regulatory sequences derived from TEs have been repurposed as enhancers, promoters, and insulators controlling host gene expression. The RAG1 and RAG2 enzymes that drive V(D)J recombination in the vertebrate adaptive immune system evolved from a transposase. Syncytin proteins, essential for placental development in mammals, derive from retroviral envelope genes. These examples illustrate a broader principle: TEs are a major source of evolutionary novelty, seeding genomes with raw material that natural selection can occasionally reshape into new functions.