TABLE 2.

Mutations in 12 ASD risk genes of zebrafish created by SFARI.

Gene name	Natural function of gene	Some results of abnormal function of mutated gene in zebrafish ASD model	References
ARID1B	Controlling and regulation of neurite outgrowth Suppressing Wnt/β-catenin signaling pathway	The imbalance of osteogenic and chondrogenic gene expression patterns Disturbance in the Wnt/β-catenin signaling pathway	(110, 111)
CHD8	Reduction in expression of genes related to Wnt/β-catenin signaling pathway	Macrocephaly Impairment in gastrointestinal motility	(112–114)
FMR1	Regulation of synaptic plasticity Regulation of neuronal protein production	Hyperactivity Anxiety like behavior Impaired inhibitory avoidance Alteration in Synaptic plasticity by reduction in long-term potentiation Craniofacial abnormalities	(115–117)
MECP2	Regulation of transcriptional repression or activation Regulation of RNA-splicing Regulation of brain function Development of neurons	Defective thigmotaxis Augmented tactile evoked potentials Low motor activity Excitation/Inhibition unbalance Decreased activity and anxiety-like behavior Shorter lifespan	(118, 119)
PTEN	Suppressing tumor Regulating metabolic pathways Regulating of neuron size	Hyperplasia Dysplasia High angiogenesis High vegfaa expression Abnormal head, tail, and notochord shapes Impaired formation of vascular network and inner ear development High levels of phosphorylated Akt Low yolk extensions	(120–123)
CNTNAP2	Cell adhesion molecules and receptors in nervous system Synaptic regulation Regulating the neuronal synchrony	Hyperactivity at nights Hypersensitivity to drug-induced seizures	(124, 125)
DYRK1A	Regulation of the growth and development of nervous tissue Increase in dendritic arborization and axon branching Neuronal trafficking Aging	Reduction in the strength of relationships and the sense of solidarity among members of a community Increasing anxiety Microcephaly Reduction in stress responses produced by hypothalamus	(126)
GRIN2B	Neural formation	Needs further investigation	(109)
NRXN1	Synapse organization Modulator of the strength of neuroligin–neurexin interactions Regulation of calcium channel activity	Reduction in blood flow Angiogenesis Low thigmotaxis Developing vain tail size Deformity of caudal vein Vascular malformation Disturbance of locomotor activity	(127, 128)
SCN2A	Encoding the voltage-gated sodium channel Regulation the action potential initiation and downstream axonal propagation	Hyperactivity Spontaneous activity of the electrograph Seizure-like behaviors Abnormal neuronal firing	(129, 130)
SHANK3	Functioning and formation of synapses Encoding scaffolding proteins at postsynaptic densities	Reduction in gastrointestinal motility Reduction in peristalsis Reduction in serotonin-expressing enteroendocrine cells Abnormal morphology Displaying repetitive behaviors Difficulties in social interactions Reduction in the number of differentiated neurons	(102, 131, 132)
SYNGAP1	Regulating of synaptic plasticity Development and proper synapse function Dendritic spine development and maturation Encoding a brain-specific synaptic Ras GTP-ase activating protein	Reduction in cell survival in the midbrain, hindbrain, and spinal cord Abnormal morphology of the brain Displaying seizure like behaviors Reduction in the number of GABAergic neurons in the midbrain and hindbrain Reduction in the number of excitatory neurons in the hindbrain	(133, 134)

CRISPR/Cas9, clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9; ENU, N-ethyl-N-nitrosourea; TALEN, Transcription activator-like effector nucleases; TNF-α, Tumor Necrosis Factor-α; ZFN, Zinc finger nucleases.