inhibitory synapses, but because of the localization only excitatory synapses are affected. Inhibition of SLITKR1 only reduces differentiation of excitatory synapses because of this. Interaction with LAR-RPTP Since they lack tyrosine phosphorylation motifs, SLITKR1 binds to LAR-RPTP through its LRR1 region in order to differentiate synapses. The LRR2 domain's function is not clearly understood yet but it is hypothesised that it is for dimerization to the cell surface. LAR-RPTP binds to the LRR1 region through its PTPδ Ig region, with 3 separate binding sites in a 1:1 binding ratio. Ig1 binds through electrostatic and hydrophobic interactions, Ig2 binds through ionic and hydrogen bonds, and Ig2 binds through hydrogen bonding. The unique properties on the concave surface are what determine which LAR-RPTP binds to it. If the proper LAR-RPTP is not bound to the LRR1 then synapse formation cannot occur, but bonding can still occur. Once they are bound properly, the complex is sufficient for synapse differentiation. Point mutations in the LRR1 region impaired differentiation as well but not binding. Clinical significance Tourette syndrome The SLITRK1 gene "is not a major risk gene for the majority of individuals" with Tourette syndrome (TS), according to a 2009 review, although its study can help contribute to our understanding of TS. Rare variants in SLITRK1 may lead to TS, and mutations in non-coding regions of SLITRK1 may also play a part, but further research needs to be done before any conclusions can be drawn. In 2005, medical researchers observed a de novo translocation on 13q in a patient with TS which broke the patient's chromosome near the SLITRK1 genome. In screening of additional patients, the authors observed a frameshift mutation in SLITRK1 in a patient with TS and the same rare ncRNA target variant (called var321 and varCDfs; target of miR-24-1) in two patients with TS. These variants were not found in several thousand controls supporting an association of the variants with TS. A subsequent examination of the region of the SLITRK1 gene found the mutation in none of 82 patients with Tourette syndrome. The authors concluded that tests to detect variant(s) in the gene probably would have little diagnostic utility. An experiment in the effects of a microdeletion in chromosome 13q31.1 was done in a fetus, the mother had passed the microdeletion to the child and both did not have tourettes or any other OCD symptoms, showing that it may not be a