Hisao Moriya

The paper uses a limit-pushing approach in yeast to measure protein abundance and toxicity, finding that overexpression tolerance varies with protein characteristics and can lead to distinct intracellular states.

The paper evaluates the neutrality of amino acid homorepeats in yeast, finding hydrophobic repeats are harmful while hydrophilic repeats suppress proteotoxic stress and define compatible sequence space.

This study identifies non-toxic proteins in yeast that can be overexpressed without growth impairment, revealing metabolic and ribosomal changes under protein burden.

The paper identifies RTMP1 as a key molecule involved in iron oxide deposition in chiton teeth through immunofluorescence and recombinant protein experiments.

This study shows that 3xGFP overproduction causes cytotoxicity through degradation overload, not aggregate formation, as it traps Hsp70 and disrupts the ubiquitin-proteasome system.

The paper improves the Z3EV promoter system to create the strongest yeast promoter, P36, which is 1.4 times stronger than TDH3 and can express up to 50% of total protein as a heterologous protein.

The paper identifies genes whose overexpression is adaptive under stress in budding yeast, revealing cellular requirements influenced by genetic background and environment.

The paper identifies genetic interactions associated with protein overproduction and nuclear export overload in yeast using genetic profiling.

The paper investigates protein-level dosage compensation in budding yeast, showing it involves multiple E3 ubiquitin ligases and N-acetyltransferases beyond the Ac/N-end rule pathway.