High impact information on MEU1

• As the cell density increases, there is a marked fall in the level of ornithine decarboxylase (ODC) in the MEU1(+) cells, which we show is caused by an antizyme-requiring degradation system [1].
• Multicopy MEU1 expression suppressed the constitutive ADH2 expression caused by cre2-1 [2].
• MEU1 is linked to PPR1 on chromosome XII [2].
• A frame shift mutation in MEU1 abolished its ability to activate UAS2-dependent gene expression [2].
• A second set of UAS2-dependent clones contained a previously uncharacterized open reading frame designated MEU1 (Multicopy Enhancer of UAS2) [2].

Biological context of MEU1

• Disruption of MEU1 reduced endogenous ADH2 expression about twofold but had no effect on cell viability or growth [2].

Associations of MEU1 with chemical compounds

• In both MEU1(+) and the meu1Delta cultures, the ODC levels were markedly decreased by the addition of spermidine to the media, and thus our results contradict the postulation of Subhi et al [1].
• The meu1Delta cells have a higher putrescine and a lower spermidine level than MEU1(+) cells, suggesting that the decreased spermidine level in the meu1Delta cultures is responsible for the greater apparent stability of ODC in the meu1Delta cells [1].
• In contrast, in MEU1+ SPE2+ cells methylthioadenosine does not accumulate and is metabolized through the methionine salvage pathway [3].

References