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PLoS One. 2013;8(3):e59887. doi: 10.1371/journal.pone.0059887. Epub 2013 Mar 21.

Polypeptone induces dramatic cell lysis in ura4 deletion mutants of fission yeast.

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1
Department of Life Science and Biotechnology, Faculty of Life and Environmental Science, Shimane University, Matsue, Japan.

Erratum in

  • PLoS One. 2013;8(8). doi:10.1371/annotation/9c5955eb-06f7-46f9-aee8-a2f8952f6747.

Abstract

Polypeptone is widely excluded from Schizosaccharomyces pombe growth medium. However, the reasons why polypeptone should be avoided have not been documented. Polypeptone dramatically induced cell lysis in the ura4 deletion mutant when cells approached the stationary growth phase, and this phenotype was suppressed by supplementation of uracil. To determine the specificity of this cell lysis phenotype, we created deletion mutants of other genes involved in de novo biosynthesis of uridine monophosphate (ura1, ura2, ura3, and ura5). Cell lysis was not observed in these gene deletion mutants. In addition, concomitant disruption of ura1, ura2, ura3, or ura5 in the ura4 deletion mutant suppressed cell lysis, indicating that cell lysis induced by polypeptone is specific to the ura4 deletion mutant. Furthermore, cell lysis was also suppressed when the gene involved in coenzyme Q biosynthesis was deleted. This is likely because Ura3 requires coenzyme Q for its activity. The ura4 deletion mutant was sensitive to zymolyase, which mainly degrades (1,3)-beta-D glucan, when grown in the presence of polypeptone, and cell lysis was suppressed by the osmotic stabiliser, sorbitol. Finally, the induction of cell lysis in the ura4 deletion mutant was due to the accumulation of orotidine-5-monophosphate. Cell wall integrity was dramatically impaired in the ura4 deletion mutant when grown in the presence of polypeptone. Because ura4 is widely used as a selection marker in S. pombe, caution needs to be taken when evaluating phenotypes of ura4 mutants.

PMID:
23555823
PMCID:
PMC3605382
DOI:
10.1371/journal.pone.0059887
[Indexed for MEDLINE]
Free PMC Article
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