Lund University: chimpanzee-specific PTERV1 retrovirus insertion silences LINC00662 gene in organoids
Researchers found that a chimpanzee-specific retroviral insertion keeps the LINC00662 gene silent, while it stays active in human brain organoids and supports neuronal development.
Researchers at Lund University, Sweden, have shown that an endogenous retrovirus inserted into the chimpanzee genome silences the gene LINC00662, which stays active in human brain organoids. The work was published in Science Advances on 23 October 2026 and was done on organoids and stem cells grown in the laboratory science.org
Science Advancesscience.orgOpen source ↗. Humans and chimpanzees diverged 5–7 million years ago and differ in brain size, structural complexity and cognitive abilities, although their protein-coding genes are highly conserved.
PTERV1 insertions in the chimpanzee genome
The retrovirus PTERV1 recently invaded the chimpanzee genome and is absent in humans. The team carried out an epigenomic analysis of PTERV1 insertions in chimpanzee neural organoids. The insertions turned out to be heavily covered by DNA methylation, forming more than 150 species-specific heterochromatin domains that can affect gene regulatory networks.
One such insertion, on chromosome 19, blocks expression of the long noncoding RNA LINC00662: DNA methylation spreads from it to the adjacent genomic region. To test causality, the authors deleted the insertion in chimpanzee induced pluripotent stem cells using CRISPR editing. Expression of LINC00662 was restored.
LINC00662 in the developing human brain
LINC00662 is a human-specific RNA that is highly expressed in the developing brain science.org
Science Advancesscience.orgOpen source ↗. According to the authors, it takes part in posttranscriptional control of neuronal maturation, axon outgrowth and neural organoid development. "The gene was strongly expressed in the human organoids, but not at all in the chimpanzee organoids," said Patricia Gerdes, a postdoctoral researcher at Lund University.
In a separate experiment, the team silenced LINC00662 in human brain organoids with CRISPR. Genes involved in nerve cell development and in the formation of connections between these cells became less active.
The authors conclude that endogenous retroviral insertions contributed to the functional divergence of human and chimpanzee brains, and describe a mechanism by which retroviral infections influenced primate brain speciation. Johan Jakobsson, professor of molecular neurogenetics at Lund University, said the team will next examine whether other viral remnants influenced brain evolution and whether such sequences are linked to brain diseases.
