Deletion of Sema3f in mouse interneurons during early development decreased the number of interneurons/neurites and mRNAs for cell-specific GABAergic markers and increased epileptogenesis and autistic behaviors (Li et al., 2019).
Molecular Function
This gene encodes a member of the semaphorin III family of secreted signaling proteins that are involved in axon guidance during neuronal development. The encoded protein contains an N-terminal Sema domain, an immunoglobulin loop and a C-terminal basic domain. This gene is expressed by the endothelial cells where it was found to act in an autocrine fashion to induce apoptosis, inhibit cell proliferation and survival, and function as an anti-tumorigenic agent.
External Links
References
Type
Title
Type of Disorder
Associated Disorders
Author, Year
Primary
Deletion of Semaphorin 3F in Interneurons Is Associated with Decreased GABAergic Neurons, Autism-like Behavior, and Increased Oxidative Stress Casc...
Selective null deletion of Sema3f in interneurons but not excitatory neurons decreased the number of interneurons and mRNAs for cell-specific GABAergic markers and increased epileptogenesis and autistic behaviors including decreased sociability, increased digging, and jumping, neuroinflammation and oxidative stress.
References
Type
Title
Author, Year
Primary
Deletion of Semaphorin 3F in Interneurons Is Associated with Decreased GABAergic Neurons, Autism-like Behavior, and Increased Oxidative Stress Casc...
Model Type:
Genetic
Model Genotype:
Homozygous
Mutation:
Mice selectively null for SEMA3F in postmitotic immature GABAergic inhibitory neurons (DLX5/6^Cre het; SEMA3F^fl/fl). Conditional ready mice, with loxP sites flanking the first exon were crossed with heterozygous Dlx5/6^Cre mice.
Allele Type: Conditional knockout
Strain of Origin: Genetic Background: C57BL/6J*FVB/NJ
ES Cell Line: Mutant ES Cell Line: Model Source: Kolodkin lab (Johns Hopkins University); Jackson Laboratory
Model Type:
Genetic
Model Genotype:
Homozygous
Mutation:
Mice selectively null for SEMA3F in excitatory neurons (Emx1^Cre het; SEMA3F^fl/fl). Conditional ready mice, with loxP sites flanking the first exon were crossed with heterozygous Emx1^Cre mice.
Allele Type: Conditional knockout
Strain of Origin: Genetic Background: C57BL/6J
ES Cell Line: Mutant ES Cell Line: Model Source: gift from Dr. Alex Kolodkin (Johns Hopkins University); Jackson Laboratory
Model Type:
Genetic
Model Genotype:
Homozygous
Mutation:
Mice selectively null for SEMA3F in neurons in the telencephalon and hypothalamus (Nkx2.1^Cre; SEMA3F^fl/fl). Conditional ready mice, with loxP sites flanking the first exon were crossed with homozygous Nkx2.1^Cre mice.
Allele Type: Conditional knockout
Strain of Origin: Genetic Background: C57BL/6J*FVB/NJ
ES Cell Line: Mutant ES Cell Line: Model Source: Kolodkin lab (Johns Hopkins University); Jackson Laboratory
Description: Mutants show decrease in inhibitory gaba positive interneurons in the hippocampus and cortex, and decrease in the number of calretinin positive interneurons in the ca1 region, compared with controls. mutants show decrease in gabra1 positive gabaergic interneurons in the hippocampus compared with controls.
Exp Paradigm: NA
Description: Mutants show decrease in neuroligin2 and gad65 staining of gabaergic synapses in the ca3 region of the hippocampus compared with controls.
Exp Paradigm: NA
Description: Mutants show decrease in inhibitory gaba neuronal marker dlx1 transcripts compared with controls, indicating a decrease in dlx1 positive inhibitory gabaergic neurons.
Exp Paradigm: NA
Description: Mutants show no change in the number of nissl stained neurons in the pyramidal layer of the hippocampus but a decrease in neurons in the dendritic layers of the hippocampus compared with controls.
Exp Paradigm: NA
Description: Mutants show increase in 4hne and dhe staining in the cortex, hippocampus and amygdala compared with controls, indicating increase in lipid peroxidation and oxidative stress.
Exp Paradigm: NA
Description: Mutants show decreased latency to ptz induced tonic clonic seizures compared with controls.
Exp Paradigm: A subconvulsant dose of ptz was administered daily for 30 days.
Electroencephalogram (eeg): signature of seizure/epilepsy1
Increased
Description: Mutants show increase in seizure events, and spike counts per hour, and decrease in latency for gtc seizures compared with controls in long term video eeg.
Exp Paradigm: NA
Description: Mutants show increased microglia activation in the hippocampus compared with controls, measured by increased iba1 staining area.
Exp Paradigm: NA
Description: Mutants show decrease in sema3f protein expression in hippocampal interneurons compared with controls, indicating deletion of sema3f in ventral telencephalic neurons during development.
Exp Paradigm: NA
Description: Mutants show decrease in inhibitory gaba positive interneurons in the somatosensory cortex but no change in inhibitory gaba positive interneurons or calretinin positive interneurons in the hippocampus compared with controls.
Exp Paradigm: NA
Description: Mutants show decreased latency to ptz induced tonic clonic seizures compared with controls.
Exp Paradigm: A subconvulsant dose of ptz was administered daily for 30 days.
Description: Mutants show decrease in sema3f protein expression in hippocampal excitatory neurons compared with controls, indicating deletion of sema3f in dorsal telencephalic neurons during development.
Exp Paradigm: NA
