In our previous study, it was found that the killer toxin produced by the marine-derived yeast Wickerhamomyces anomalus YF07b has both killing activity and β-1,3-glucanase activity and the molecular mass of it is 47.0 kDa. In this study, the same yeast strain was found to produce another killer toxin which only had killing activity against some yeast strains, but had no β-1,3-glucanase activity and the molecular mass of the purified killer toxin was 67.0 kDa. The optimal pH, temperature and NaCl concentration for action of the purified killer toxin were 3.5, 16 °C and 4.0 % (w/v), respectively. The purified killer toxin could be bound by the whole sensitive yeast cells, but was not bound by manann, chitin and β-1,3-glucan. The purified killer toxin had killing activity against Yarrowia lipolytica, Saccharomyces cerevisiae, Metschnikowia bicuspidata WCY, Candida tropicalis, Candida albicans and Kluyveromyces aestuartii. Lethality of the sensitive cells treated by the newly purified killer toxin from W. anomalus YF07b involved disruption of cellular integrity by permeabilizing cytoplasmic membrane function.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10482-012-9855-3 | DOI Listing |
Future Microbiol
December 2024
Department of Biology, Faculty of Biological Sciences, Falavarjan Branch, Islamic Azad University, Isfahan, Iran.
Aim: Leishmaniasis is a globally prevalent parasitic disease that has drawn significant attention. Killer yeasts offer a novel biological control method, presenting a potential alternative for treating leishmaniasis. This study evaluates the antileishmanial activity of and killer toxins against .
View Article and Find Full Text PDFACS Pharmacol Transl Sci
December 2024
National Key Laboratory of Green Pesticide, International Joint Research Center for Intelligent Biosensing Technology and Health, College of Chemistry, Central China Normal University, Wuhan 430079, China.
The tumor-associated antigen MUC1 is an attractive target for immunotherapy, however, its weak immunogenicity limits the induction of antitumor immune responses. To overcome this limitation, in this study, MUC1 glycopeptide was covalently linked with a diphtheria toxin-derived T-helper epitope (DT). Subsequently, the resulting DT-MUC1 glycopeptide was physically mixed with natural killer T cell agonist αGalCer to explore their immunomodulatory synergy.
View Article and Find Full Text PDFPLoS One
November 2024
Food Microbiology Unit, Miyagi University School of Food Industrial Sciences, Sendai, Japan.
Hansenula mrakii killer toxin resistant gene 1 (HKR1) is an intronless, single-exon gene that encodes Hkr1, the signaling mucin of the budding yeast Saccharomyces cerevisiae. HKR1 overexpression confers S. cerevisiae cells with resistance to the HM-1 killer toxin produced by the killer yeast Hansenula mrakii (currently known as Cyberlindnera mrakii).
View Article and Find Full Text PDFJ Reprod Immunol
December 2024
Perm Federal Research Center, Institute of Ecology and Genetics of Microorganisms, Ural Branch of the Russian Academy of Sciences, Perm 614081, Russia.
Estriol (E) is one of hormones whose synthesis is mainly associated with pregnancy. The hormone can also regulate immune cells functions. E influence on monocyte indoleamine-2,3-dioxygenase (IDO1) activity and Treg and NK cells' markers expression was investigated.
View Article and Find Full Text PDFClin Nutr
December 2024
Epidemiology, Medical Faculty, University of Augsburg, Stenglinstraße 2, 86156 Augsburg, Germany.
Aims: The pathophysiology of diabetes is not fully understood; recent research indicates close relations with immunological alterations. Therefore, the aim of this study was to investigate the associations between markers of glucose metabolism and characteristics of blood lymphocytes in a population-based cohort.
Methods: The analysis was based on data from 219 non-diabetic participants of the MEGA study in Augsburg, Germany, who were recruited between 2018 and 2021.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!