An ancient piece of viral DNA called an Alu element gets spliced into the human IFNAR2 gene, creating a shortened version of this key immune receptor. The resulting "decoy" protein is secreted from cells and intercepts interferon signals, acting as a natural brake on the immune response.

Ancient retroviruses called LTR10 elements stay silent in healthy cells but reawaken in colorectal cancer, where they act as rogue gene switches driven by the MAPK signaling pathway. Treating tumors with MEK inhibitor drugs shuts these viral switches back off, pointing to a possible new therapeutic angle.

Blocking the gene-silencing enzymes EHMT1 and EHMT2 causes therapy-resistant ovarian tumors to shrink. The drugs work by reawakening tumor suppressor genes that the cancer had switched off to evade treatment.

An ancient retrovirus embedded in the human genome acts as a hidden gene switch that turns on the immune regulator SP140 specifically in tumors. The finding adds SP140 to a growing list of cancer-relevant genes hijacked by reactivated viral DNA.

Pairing EHMT inhibitors (which target gene-silencing enzymes) with PARP inhibitors (which block DNA repair) kills therapy-resistant ovarian cancer cells far better than either drug alone. The combination could help patients whose tumors have stopped responding to standard PARP inhibitor treatment.

A LINE-1 transposon sitting inside the IFNAR1 gene helps control how much of this interferon receptor immune cells produce. The work shows that even "parasitic" DNA insertions can be domesticated to fine-tune neighboring immune genes.

Short repetitive DNA elements called B2 SINEs, found only in rodent genomes, were co-opted as gene enhancers that fire up during the antiviral immune response in mice. This mirrors similar discoveries in primates and cattle, suggesting that different mammals have independently repurposed different transposable elements to wire up their immune systems.

Transposable elements unique to cattle and their relatives — LINE-2 and Bov-A3 — were repurposed as immune gene switches that activate during viral infection. The finding extends transposon co-option as a regulatory innovation beyond primates and rodents to a third major mammalian lineage.

Transposable elements in bat genomes are dynamically switched on and off during the interferon antiviral response. Because bats tolerate many viruses without getting sick, these regulatory changes may help explain their unusual immune resilience.

Ancient retroviruses from the MER41 family carry built-in binding sites for immune transcription factors, and were co-opted as gene enhancers that turn on innate immune genes like AIM2 and APOL1 during interferon signaling. Deleting these viral remnants with CRISPR shuts off the immune response at their target genes — proving they are essential regulators, not junk DNA.

A review of how evolutionary perspectives illuminate placental biology and pregnancy-related disease. Highlights how rapid placental innovation and genetic conflicts between mother and fetus shape both normal pregnancy and its complications.

Endogenous retroviruses embedded in mammalian genomes function as species-specific gene enhancers in the placenta. This may help explain why the placenta is one of the most rapidly evolving organs across mammals — viral DNA provides a ready supply of regulatory variation.

Proteins expressed at the interface between mother and fetus in rodents evolve at unusually fast rates. The pattern fits the theory of parent-offspring genetic conflict, where maternal and paternal interests over fetal resource allocation drive an evolutionary arms race.

Maps how chromatin — the protein packaging of DNA — and transcription factor binding change across early vertebrate development. The dataset reveals how regulatory landscapes are reorganized as embryos lay down their body plan.

A comprehensive review synthesizing evidence that transposable elements — long dismissed as genomic parasites — are a major source of new regulatory DNA across animal genomes. Covers TE-derived enhancers, promoters, and insulators, and the evolutionary forces that turn parasitic sequences into functional control elements.

Reviews how endogenous retroviruses serve as platforms for epigenetic regulation of immune genes. Walks through the mechanisms by which retrovirus-derived chromatin marks and binding sites tune immune cell behavior.

A commentary on new work showing that transposable elements provide critical binding sites for the transcription factors that establish T cell identity. Highlights how the immune system has been built, in part, on a foundation of parasitic DNA.

A perspective on how endogenous retroviruses — relics of ancient infections in our ancestors — became domesticated into essential regulators of placental gene expression. Argues that placental biology is fundamentally a story of host-virus integration.

Argues that endogenous retroviruses have been a major driving force behind placental evolution by donating species-specific regulatory elements to host genomes. Provides a framework for understanding why the placenta differs so dramatically across mammals.

A commentary on new work showing that transposable elements contribute to X chromosome dosage compensation — the cellular mechanism that balances gene expression from the two sex chromosomes. Another example of how parasitic DNA gets repurposed for fundamental cellular functions.