Mitotic defects in fission yeast lipid metabolism 'cut' mutants are suppressed by ammonium chloride
Jazyk angličtina Země Anglie, Velká Británie Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
29931271
PubMed Central
PMC6037054
DOI
10.1093/femsyr/foy064
PII: 5040229
Knihovny.cz E-zdroje
- MeSH
- acetyl-CoA-karboxylasa genetika MeSH
- chlorid amonný chemie metabolismus farmakologie MeSH
- fenotyp MeSH
- kultivační média chemie MeSH
- lipidová tělíska účinky léků metabolismus MeSH
- metabolismus lipidů účinky léků genetika MeSH
- mitóza účinky léků genetika MeSH
- mutace MeSH
- penetrance MeSH
- Schizosaccharomyces pombe - proteiny genetika MeSH
- Schizosaccharomyces účinky léků genetika růst a vývoj metabolismus MeSH
- transkripční faktory genetika MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- acetyl-CoA-karboxylasa MeSH
- Cbf11 protein, S pombe MeSH Prohlížeč
- chlorid amonný MeSH
- kultivační média MeSH
- Schizosaccharomyces pombe - proteiny MeSH
- transkripční faktory MeSH
Fission yeast 'cut' mutants show defects in temporal coordination of nuclear division with cytokinesis, resulting in aberrant mitosis and lethality. Among other causes, the 'cut' phenotype can be triggered by genetic or chemical perturbation of lipid metabolism, supposedly resulting in shortage of membrane phospholipids and insufficient nuclear envelope expansion during anaphase. Interestingly, penetrance of the 'cut' phenotype in mutants of the transcription factor cbf11 and acetyl-coenzyme A carboxylase cut6, both related to lipid metabolism, is highly dependent on growth media, although the specific nutrient(s) affecting 'cut' occurrence is not known. In this study, we set out to identify the growth media component(s) responsible for 'cut' phenotype suppression in Δcbf11 and cut6-621 cells. We show that mitotic defects occur rapidly in Δcbf11 cells upon shift from the minimal EMM medium ('cut' suppressing) to the complex YES medium ('cut' promoting). By growing cells in YES medium supplemented with individual EMM components, we identified ammonium chloride, an efficiently utilized nitrogen source, as a specific and potent suppressor of the 'cut' phenotype in both Δcbf11 and cut6-621. Furthermore, we found that ammonium chloride boosts lipid droplet formation in wild-type cells. Our findings suggest a possible involvement of nutrient-responsive signaling in 'cut' suppression.
Department of Cell Biology Faculty of Science Charles University Prague Czech Republic
Department of Radiation Biology Institute for Cancer Research Oslo University Hospital Oslo Norway
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