以下の総説が発行されました。

Sasaki T, Takei Y. Localization Mechanism of Myosin Id, an ASD Risk Gene Product in Dendritic Spines. Jap J Biol Psych. 2020, 31(2) 93-97.

Dendritic spines, the postsynaptic compartments at excitatory synapses, are capable of changing their shape and size to modulate synaptic transmission. The actin cytoskeleton and a variety of actin︲binding proteins play a critical role in the dynamics of dendritic spines. Abnormalities of spine dynamics are implicated in several psychiatric disorders. Class I myosins are monomeric motor proteins that move along actin filaments using the energy of ATP hydrolysis. Of these class I myosins, myosin Id has been reported to be expressed in neurons, whereas its subcellular localization in neurons remained unknown. The linkage analysis suggests that myosin Id is a potential risk gene for autism spectrum disorder（ASD）. Here, we investigated the subcellular localization of myosin Id and determined the domain responsible for it. We found that myosin Id is enriched in the dendritic spines of primary hippocampal neurons. The mutant form lacking the TH1 domain is
less distributed in dendritic spines than is the full︲length form. Taken together, our findings reveal that myosin Id localizes in dendritic spines through the TH1 domain. These results provide the first clues to understand the role of this molecule in the development and pathophysiology of ASD.

ミオシンはアクチンと結合する分子モーターである。ミオシン Id は自閉スペクトラム症のリスク遺伝子であり，神経細胞での局在や機能は不明である。培養神経細胞に EGFP 融合ミオシン Id を発現させたところ，樹状突起スパインに集積が認められ，この局在には TH1 ドメインが重要であることが判明した。本研究結果は，自閉スペクトラム症発現・病態における本分子の役割を理解する最初の手がかりを与えると考えられる。