= Koreaki Ito
{c}
Koreaki Ito is a researcher in <protein secretion> and the relationship between <translation (biology)> and the emerging <nascent chain>. With <Hitoshi Nakatogawa>, he showed that the <ribosomal exit tunnel> can participate in recognizing the sequence of a growing <protein>, rather than simply providing a passive passage out of the <ribosome>.<The ribosomal exit tunnel functions as a discriminating gate by Hitoshi Nakatogawa and Koreaki Ito>[Cell 108, 629–636 (2002), Abstract and published byline]{ref}
Their <SecM> study connected two kinds of evidence. An arrest-causing sequence in the <nascent chain> produced <ribosome stalling>, while <suppressor mutations> in <23S ribosomal RNA> or <ribosomal protein L22> allowed elongation to continue. The altered residues faced the tunnel constriction. This localization supported an interaction between the tunnel and the emerging chain.<The ribosomal exit tunnel functions as a discriminating gate by Hitoshi Nakatogawa and Koreaki Ito>[Abstract: arrest sequence and tunnel-facing suppressor mutations]{ref}
A simplified experiment illustrates why suppressing a phenotype is informative but does not, by itself, prove a direct physical contact. Compare four combinations: ordinary versus altered <SecM>, each translated by ordinary versus altered <ribosomes>. If an altered <ribosome> restores elongation specifically for the arresting sequence, the result links the two components functionally. A general reduction in <translation (biology)> could instead change the apparent abundance of every product; comparing only one final band would miss that alternative. Spatial information about the changed <ribosomal RNA> and <protein> residues adds another constraint. Even then, a <suppressor mutation> might act by changing a nearby conformation rather than removing a direct contact. The experiment is powerful because genetic and structural evidence constrain one another, while leaving room to test the detailed physical mechanism.
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