<真核生物からのアプローチ>細胞内環境などに応答してプログラムされた翻訳アレストを引き起こす機能性翻訳途上鎖は,近年,真核生物においても報告が増えつつある。機能性翻訳途上鎖は,リボソームの出口トンネル,中でも出口トンネル内にリボソームタンパク質のuL4とuL22が突き出た「狭窄部位」と相互作用することで,翻訳アレストを引き起こすと考えられている。
これまでの研究で,シロイヌナズナのuL4が出口トンネルに突き出たβ-ループの頂点近くに位置するArg-77のアラニン置換(R77A),もしくは,これを挟むThr-75とVal-79の欠失(ΔTV)を導入した変異型リボソームを持つ株を作出している。これら変異株から調製した試験管内翻訳系を用いた解析により,真核生物で報告されている機能性翻訳途上鎖への効果を調べた結果,変異の影響はそれぞれに異なっており,uL4との相互作用の違いを示すと考えられる(図; 論文1)。本研究では,uL22への変異導入やuL4の他の部位への変異導入に挑戦するとともに,真核生物が持つ他の機能性翻訳途上鎖の解析へと展開し,機能性翻訳途上鎖とリボソーム出口トンネルの相互作用を明らかにしたい。
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