Mutations in the autism-linked gene PAX5 underlie a range of traits, including developmental delay, intellectual disability, seizures and autism.

The fact that autism seems to affect more boys than girls is often attributed to diagnostic gaps, but the skew remains largely unexplained. Some scientists are turning to basic biology for answers.

Activating the immune system blunts social behavior in mice missing a copy of the autism-linked gene SHANK3, according to a new study. Blocking TRPV4, which encodes an ion channel involved in inflammatory responses, can reverse this effect.

Mutations in all three accelerate the maturation of inhibitory neurons, which could upset the brain’s balance of excitation and inhibition early in development.

Model animals don’t develop the usual behavioral and motor problems when reared in an enclosure containing exercise wheels, toys and treats.

Some copy number variants may boost a person’s chances of having autism, but to a lesser extent than previously thought.

Mice missing a copy of the gene ASH1L have excess synapses and autism-like behavioral differences, some of which are reversed by boosting an ASH1L-regulated gene.

Loss of the POGZ gene in mice makes certain genes inaccessible and prevents their expression.

Autism may involve different levels of RNA isoforms encoded by genes in the brain, which express many more proteins than previously thought.

In mice with a mutated copy of SHANK3, stress induces social deficits and alters gene expression in certain excitatory neurons. But eliminating a stress-related protein that regulates SHANK3 restores typical social functioning in the animals.