| First Author | Xing L | Year | 2021 |
| Journal | EMBO J | Volume | 40 |
| Issue | 13 | Pages | e107093 |
| PubMed ID | 33938018 | Mgi Jnum | J:308527 |
| Mgi Id | MGI:6729786 | Doi | 10.15252/embj.2020107093 |
| Citation | Xing L, et al. (2021) Expression of human-specific ARHGAP11B in mice leads to neocortex expansion and increased memory flexibility. EMBO J 40(13):e107093 |
| abstractText | Neocortex expansion during human evolution provides a basis for our enhanced cognitive abilities. Yet, which genes implicated in neocortex expansion are actually responsible for higher cognitive abilities is unknown. The expression of human-specific ARHGAP11B in embryonic/foetal mouse, ferret and marmoset neocortex was previously found to promote basal progenitor proliferation, upper-layer neuron generation and neocortex expansion during development, features commonly thought to contribute to increased cognitive abilities. However, a key question is whether this phenotype persists into adulthood and if so, whether cognitive abilities are indeed increased. Here, we generated a transgenic mouse line with physiological ARHGAP11B expression that exhibits increased neocortical size and upper-layer neuron numbers persisting into adulthood. Adult ARHGAP11B-transgenic mice showed altered neurobehaviour, notably increased memory flexibility and a reduced anxiety level. Our data are consistent with the notion that neocortex expansion by ARHGAP11B, a gene implicated in human evolution, underlies some of the altered neurobehavioural features observed in the transgenic mice, such as the increased memory flexibility, a neocortex-associated trait, with implications for the increase in cognitive abilities during human evolution. |
