scholarly journals Global Analysis of Saccharomyces cerevisiae Growth in Mucin

Author(s):  
Kevin Mercurio ◽  
Dylan Singh ◽  
Elizabeth Walden ◽  
Kristin Baetz

Abstract Metagenomic profiling of the human gut microbiome has discovered DNA from dietary yeasts like Saccharomyces cerevisiae. However, it is unknown if the S. cerevisiae detected by common metagenomic methods are from dead dietary sources, or from live S. cerevisiae colonizing the gut similar to their close relative Candida albicans. While S. cerevisiae can adapt to minimal oxygen and acidic environments, it has not been explored whether this yeast can metabolize mucin, the large, gel-forming, highly glycosylated proteins representing a major source of carbon in the gut mucosa. We reveal that S. cerevisiae can utilize mucin as their main carbon source, as well as perform both a transcriptome analysis and a chemogenomic screen to identify biological pathways required for this yeast to grow optimally in mucin. In total, 739 genes demonstrate significant differential expression in mucin culture, and deletion of 21 genes impact growth in mucin. Both screens suggest that mitochondrial function is required for proper growth in mucin, and through secondary assays we determine that mucin exposure induces mitogenesis and cellular respiration. We further show that deletion of an uncharacterized ORF, YCR095W-A, led to dysfunction in mitochondrial morphology and oxygen consumption in mucin. Lastly, we demonstrate that Yps7, an aspartyl protease and homologue to mucin-degrading proteins in C. albicans, is important for growth on mucin. Collectively, our work serves as the initial step towards establishing how this common dietary fungus can survive in the mucus environment of the human gut.

2019 ◽  
Vol 16 (12) ◽  
pp. 1348-1353
Author(s):  
Huanhuan Qu ◽  
Baixue Li ◽  
Jingyi Yang ◽  
Huaiwen Liang ◽  
Meixia Li ◽  
...  

Background: Disaccharide core 1 (Galβ1-3GalNAc) is a common O-glycan structure in nature. Biochemical studies have confirmed that the formation of the core 1 structure is an important initial step in O-glycan biosynthesis and it is of great importance for human body. Objective: Our study will provide meaningful and useful sights for O-glycan synthesis and their bioassay. And all the synthetic glycosides would be used as intermediate building blocks in the scheme developed for oligosaccharide construction. Methods: In this article, we firstly used chemical procedures to prepare core 1 and its derivative, and a novel disaccharide was efficiently synthesized. The structures of the synthesized compounds were elucidated and confirmed by 1H NMR, 13C NMR and MS. Then we employed three human gut symbionts belonging to Bacteroidetes, a predominantphyla in the distal gut, as models to study the bioactivity of core 1 and its derivative on human gut microbiota. Results: According to our results, both core 1 and derivative could support the growth of B. fragilis, especially the core 1 derivative, while failed to support the growth of B. thetaiotaomicron and B. ovatus. Conclusion: This suggested that the B. fragilis might have the specificity glycohydrolase to cut the glycosidic bond for acquiring monosaccharide.


Genetics ◽  
2002 ◽  
Vol 162 (3) ◽  
pp. 1147-1156 ◽  
Author(s):  
Theodor Hanekamp ◽  
Mary K Thorsness ◽  
Indrani Rebbapragada ◽  
Elizabeth M Fisher ◽  
Corrine Seebart ◽  
...  

Abstract In the yeast Saccharomyces cerevisiae, certain mutant alleles of YME4, YME6, and MDM10 cause an increased rate of mitochondrial DNA migration to the nucleus, carbon-source-dependent alterations in mitochondrial morphology, and increased rates of mitochondrial DNA loss. While single mutants grow on media requiring mitochondrial respiration, any pairwise combination of these mutations causes a respiratory-deficient phenotype. This double-mutant phenotype allowed cloning of YME6, which is identical to MMM1 and encodes an outer mitochondrial membrane protein essential for maintaining normal mitochondrial morphology. Yeast strains bearing null mutations of MMM1 have altered mitochondrial morphology and a slow growth rate on all carbon sources and quantitatively lack mitochondrial DNA. Extragenic suppressors of MMM1 deletion mutants partially restore mitochondrial morphology to the wild-type state and have a corresponding increase in growth rate and mitochondrial DNA stability. A dominant suppressor also suppresses the phenotypes caused by a point mutation in MMM1, as well as by specific mutations in YME4 and MDM10.


1999 ◽  
Vol 19 (5) ◽  
pp. 3435-3442 ◽  
Author(s):  
Gregor Steglich ◽  
Walter Neupert ◽  
Thomas Langer

ABSTRACT Prohibitins comprise a protein family in eukaryotic cells with potential roles in senescence and tumor suppression. Phb1p and Phb2p, members of the prohibitin family in Saccharomyces cerevisiae, have been implicated in the regulation of the replicative life span of the cells and in the maintenance of mitochondrial morphology. The functional activities of these proteins, however, have not been elucidated. We demonstrate here that prohibitins regulate the turnover of membrane proteins by the m-AAA protease, a conserved ATP-dependent protease in the inner membrane of mitochondria. The m-AAA protease is composed of the homologous subunits Yta10p (Afg3p) and Yta12p (Rca1p). Deletion ofPHB1 or PHB2 impairs growth of Δyta10 or Δyta12 cells but does not affect cell growth in the presence of the m-AAA protease. A prohibitin complex with a native molecular mass of approximately 2 MDa containing Phb1p and Phb2p forms a supercomplex with them-AAA protease. Proteolysis of nonassembled inner membrane proteins by the m-AAA protease is accelerated in mitochondria lacking Phb1p or Phb2p, indicating a negative regulatory effect of prohibitins on m-AAA protease activity. These results functionally link members of two conserved protein families in eukaryotes to the degradation of membrane proteins in mitochondria.


2003 ◽  
Vol 124 (4) ◽  
pp. A155-A156
Author(s):  
Kevin Gurney ◽  
Julie Elliott ◽  
Hoorig Nassanian ◽  
Ian McGowan ◽  
Carol Song ◽  
...  
Keyword(s):  

2021 ◽  
Vol 10 (13) ◽  
pp. e235101321263
Author(s):  
Bruno Santos Francisco ◽  
Felipe Bueno Dutra ◽  
Emerson Viveiros ◽  
Raquel Passaretti ◽  
Rafael Paranhos Martins ◽  
...  

In Brazil, most degraded areas are occupied by exotic and invasive species, which require alternatives for their management. We evaluated the allelopathic effects of Waltheria indica in the laboratory from aqueous extracts of leaves and roots on the germination of the species Lactuca sativa L. (lettuce), Urochloa brizantha (Hochst. ex A.Rich.) RDWebster (brachiaria) and Handroanthus chrysotrichus (Mart. ex DC.) Mattos (yellow Ipe). We collected adult one-year-old Waltheria indica shrubs in ecological restoration areas by direct seeding. We used two treatments with aqueous extracts of leaves and roots and a control without extract, with ten repetitions of 10 seeds per treatment, totaling 600 seeds per test species. Germination and use of tetrazolium assays to evaluate the potential respiratory activity of the roots were used. The aqueous extract of W.indica leaves affected the number of germinated seeds of all test species, while the aqueous extract of roots affected only L. sativa and H. chrysotrichus. There were no significant differences between treatments (leaf and root extracts) in species germination. The aqueous extracts of Waltheria indica leaves and roots affected germination and cellular respiration of the studied species, mainly in Lactuca sativa. The identification of W. indica allelopathic compounds may be an initial step so that in the future new bioherbicides are produced from extracts of this species, or even that its seeds can be sown together with non-sensitive native species, aiming for control of exotic species in ecological restoration projects.


2018 ◽  
Vol 101 (4) ◽  
pp. 1119-1126 ◽  
Author(s):  
Abdullah A Alyousef

Abstract The bacterium originally named Bacillus difficilis was later renamed Clostridium difficile because of the difficulty associated with its isolation in the laboratory. C. difficile causes human-associated diarrhea, which is now known as C. difficile infection (CDI), a major cause of nosocomial infection mainly occurring in developed countries. Changes in antibiotic patterns in its strains produce toxins that are responsible for the high mortality rates associated with CDI; therefore, the epidemiology and severity of CDI have recently changed. Apart from CDI, C. difficile also causes opportunistic infections of the human gut usually when the normal gut flora are disrupted by broad-spectrum antibiotics. By disrupting normal gut flora, spores of C. difficile germinate and traverse the gut mucosa through flagellar binding to the mucosal epithelium where several proteins are involved in the binding of C. difficile. Proper diagnostic techniques have to be applied to ensure early identification of CDI and prompt treatment administered because false results may lead to inappropriate treatment and increase risk of cross-infection. This review discusses the epidemiology and pathogenicity of this bacterium with concern for its changing pattern over the years. Further details on the diagnosis of CDI are elaborated upon, mainly focusing on the limits of and challenges in molecular diagnosis.


1998 ◽  
Vol 18 (7) ◽  
pp. 4043-4052 ◽  
Author(s):  
Karen H. Berger ◽  
Michael P. Yaffe

ABSTRACT Phb2p, a homolog of the tumor suppressor protein prohibitin, was identified in a genetic screen for suppressors of the loss of Mdm12p, a mitochondrial outer membrane protein required for normal mitochondrial morphology and inheritance in Saccharomyces cerevisiae. Phb2p and its homolog, prohibitin (Phb1p), were localized to the mitochondrial inner membrane and characterized as integral membrane proteins which depend on each other for their stability. In otherwise wild-type genetic backgrounds, null mutations in PHB1 andPHB2 did not confer any obvious phenotypes. However, loss of function of either PHB1 or PHB2 in cells with mitochondrial DNA deleted led to altered mitochondrial morphology, and phb1 or phb2 mutations were synthetically lethal when combined with a mutation in any of three mitochondrial inheritance components of the mitochondrial outer membrane, Mdm12p, Mdm10p, and Mmm1p. These results provide the first evidence of a role for prohibitin in mitochondrial inheritance and in the regulation of mitochondrial morphology.


Sign in / Sign up

Export Citation Format

Share Document