en.wikipedia.org/wiki/Zilong_Qiu
2 corrections found
showed autistic behaviour (Rett syndrome)
The 2016 monkey study was a model of MECP2 duplication syndrome, not Rett syndrome. A distinct Rett-syndrome monkey model was reported later, in 2017, using MECP2 loss-of-function editing.
Full reasoning
The article conflates two different MECP2-related disorders.
Qiu's 2016 Nature paper says the monkeys overexpressed human MeCP2 and frames the work around MECP2 duplication syndrome, whose symptoms overlap with autism. Its abstract states: "Duplications of MECP2-containing genomic segments cause the MECP2 duplication syndrome" and then reports "transgenic cynomolgus monkeys ... expressing human MeCP2 in the brain" that exhibit autism-like behaviours.
That is not the same as Rett syndrome. Rett syndrome is classically caused by loss-of-function mutations in MECP2, and a separate 2017 paper explicitly reported "TALEN-edited MECP2 mutant cynomolgus monkeys serving as a model for ... Rett syndrome (RTT)."
So the page is wrong to label the 2016 autism-like transgenic monkeys as "Rett syndrome"; that 2016 result modeled MECP2 duplication syndrome, while the monkey Rett model was reported later in 2017.
2 sources
- Autism-like behaviours and germline transmission in transgenic monkeys overexpressing MeCP2 | Nature
Duplications of MECP2-containing genomic segments cause the MECP2 duplication syndrome ... Here we report that lentivirus-based transgenic cynomolgus monkeys expressing human MeCP2 in the brain exhibit autism-like behaviours.
- Modeling Rett Syndrome Using TALEN-Edited MECP2 Mutant Cynomolgus Monkeys | PubMed
Here, we report detailed genotypes and phenotypes of TALEN-edited MECP2 mutant cynomolgus monkeys serving as a model for a neurodevelopmental disorder, Rett syndrome (RTT), which is caused by loss-of-function mutations in the human MECP2 gene.
using gene manipulation method called base editing in mice and monkeys.
The 2026 Nature study repaired the CHD3 mutation in a mouse model, not in monkeys. The primate experiments only showed delivery/editor reconstitution in monkey brains to support translational feasibility.
Full reasoning
This sentence overstates what the 2026 Nature paper accomplished in nonhuman primates.
In the paper itself, the mutation correction is reported in a humanized mouse model: the authors write that they modeled the recurrent CHD3 variant in mice and achieved efficient on-target base correction, restoring CHD3 levels and improving behavioural abnormalities in mice.
For monkeys, the paper describes something narrower: "intrathecal dual AAV delivery in nonhuman primates resulted in widespread neuronal transduction and efficient TeABE reconstitution, a result that supports its translational feasibility." In other words, the monkey experiments were used to assess delivery and feasibility, not to show repair of a pathogenic CHD3 mutation in monkeys.
A companion Nature News & Views likewise summarizes the work as a gene-editing approach that "restores CHD3 function in mice harbouring a mutation". So the article is inaccurate in saying the mutation was repaired "in mice and monkeys."
2 sources
- In vivo base editing of Chd3 rescues behavioural abnormalities in mice | Nature
Here we show that modelling the recurrent CHD3 variant p.R1025W in a humanized mouse model ... achieved efficient on-target correction ... Furthermore, intrathecal dual AAV delivery in nonhuman primates resulted in widespread neuronal transduction and efficient TeABE reconstitution, a result that supports its translational feasibility.
- Gene editing treats a mouse model of a neurodevelopmental disorder | Nature
Yang et al. have developed a gene-editing approach ... that restores CHD3 function in mice harbouring a mutation that is commonly observed in children with the disorder.