scholarly journals Bite size ofCaenorhabditis elegansregulates feeding, satiety and development on yeast diet

2018 ◽  
Author(s):  
Atreyee De ◽  
Amit K Sahu ◽  
Varsha Singh

ABSTRACTIn the wild, the soil dwellingnematode Caenorhabditis elegansprimarily feeds on microbes which are abundant in rotting vegetation. Recent published studies showthat several Gram-positive and Gram-negative bacterial populations predominantly constitutes theC. elegansgut microbiome but surprisingly lack any yeast species. Here, we show thatC. elegansdisplay low satiety on yeast diet ofCryptococcus neoformans, C. laurentiiorS. cerevisiae. We found that average size of budding yeast cells is much larger thanE. colicells. Yeast cells also cause pharyngeal obstruction, diminished feeding, and lower level of neutral lipids in adultC. elegans. Using scanning electron microscopy, we show that the mouth size ofC. eleganslarvae is smaller than average yeast cell. The larvae have no detectable yeast in their alimentary canal and they undergo delayed development on yeast diet. We propose that microbial cell size or bite size could be one of the crucial factors in regulation of feeding inC. elegans.IMPORTANCEThe microbiome inC. elegansgut is composed of diverse genera of bacteria but it lacks yeast and other fungi. In this study, we provide evidence that yeast cell size is bigger than the mouth size ofC. eleganslarvae. We propose that “bigger than the bite’’ size of yeast cells is one possible reason for low satiety on yeast diet, reduced feeding, lower stored lipids and delayed development. The bite size threshold imposed byC. elegansmouth can, partly, explain absence of yeast inC. elegansnative gut microbiome and “bite size’’ can be studied further as a determinant of microbiome diversity in other animals.

2021 ◽  
Vol 7 (7) ◽  
pp. 520
Author(s):  
Jianmin Fu ◽  
Nohelli E. Brockman ◽  
Brian L. Wickes

The transformation of Cryptococcus spp. by Agrobacterium tumefaciens has proven to be a useful genetic tool. A number of factors affect transformation frequency. These factors include acetosyringone concentration, bacterial cell to yeast cell ratio, cell wall damage, and agar concentration. Agar concentration was found to have a significant effect on the transformant number as transformants increased with agar concentration across all four serotypes. When infection time points were tested, higher agar concentrations were found to result in an earlier transfer of the Ti-plasmid to the yeast cell, with the earliest transformant appearing two h after A. tumefaciens contact with yeast cells. These results demonstrate that A. tumefaciens transformation efficiency can be affected by a variety of factors and continued investigation of these factors can lead to improvements in specific A. tumefaciens/fungus transformation systems.


Metabolites ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 456
Author(s):  
Pejman Salahshouri ◽  
Modjtaba Emadi-Baygi ◽  
Mahdi Jalili ◽  
Faiz M. Khan ◽  
Olaf Wolkenhauer ◽  
...  

The human gut microbiota plays a dual key role in maintaining human health or inducing disorders, for example, obesity, type 2 diabetes, and cancers such as colorectal cancer (CRC). High-throughput data analysis, such as metagenomics and metabolomics, have shown the diverse effects of alterations in dynamic bacterial populations on the initiation and progression of colorectal cancer. However, it is well established that microbiome and human cells constantly influence each other, so it is not appropriate to study them independently. Genome-scale metabolic modeling is a well-established mathematical framework that describes the dynamic behavior of these two axes at the system level. In this study, we created community microbiome models of three conditions during colorectal cancer progression, including carcinoma, adenoma and health status, and showed how changes in the microbial population influence intestinal secretions. Conclusively, our findings showed that alterations in the gut microbiome might provoke mutations and transform adenomas into carcinomas. These alterations include the secretion of mutagenic metabolites such as H2S, NO compounds, spermidine and TMA, as well as the reduction of butyrate. Furthermore, we found that the colorectal cancer microbiome can promote inflammation, cancer progression (e.g., angiogenesis) and cancer prevention (e.g., apoptosis) by increasing and decreasing certain metabolites such as histamine, glutamine and pyruvate. Thus, modulating the gut microbiome could be a promising strategy for the prevention and treatment of CRC.


1995 ◽  
Vol 15 (7) ◽  
pp. 3487-3495 ◽  
Author(s):  
M P Draper ◽  
C Salvadore ◽  
C L Denis

The CCR4 protein from Saccharomyces cerevisiae is a component of a multisubunit complex that is required for the regulation of a number of genes in yeast cells. We report here the identification of a mouse protein (mCAF1 [mouse CCR4-associated factor 1]) which is capable of interacting with and binding to the yeast CCR4 protein. The mCAF1 protein was shown to have significant similarity to proteins from humans, Caenorhabditis elegans, Arabidopsis thaliana, and S. cerevisiae. The yeast gene (yCAF1) had been previously cloned as the POP2 gene, which is required for expression of several genes. Both yCAF1 (POP2) and the C. elegans homolog of CAF1 were shown to genetically interact with CCR4 in vivo, and yCAF1 (POP2) physically associated with CCR4. Disruption of the CAF1 (POP2) gene in yeast cells gave phenotypes and defects in transcription similar to those observed with disruptions of CCR4, including the ability to suppress spt10-enhanced ADH2 expression. In addition, yCAF1 (POP2) when fused to LexA was capable of activating transcription. mCAF1 could also activate transcription when fused to LexA and could functionally substitute for yCAF1 in allowing ADH2 expression in an spt10 mutant background. These data imply that CAF1 is a component of the CCR4 protein complex and that this complex has retained evolutionarily conserved functions important to eukaryotic transcription.


2020 ◽  
Vol 309 ◽  
pp. 125700 ◽  
Author(s):  
Stephen Young ◽  
Rewa Rai ◽  
Nitin Nitin

2020 ◽  
Vol 31 (10) ◽  
pp. 1069-1084 ◽  
Author(s):  
Heidi M. Blank ◽  
Ophelia Papoulas ◽  
Nairita Maitra ◽  
Riddhiman Garge ◽  
Brian K. Kennedy ◽  
...  

In several systems, including budding yeast, cell cycle-dependent changes in the transcriptome are well studied. In contrast, few studies queried the proteome during cell division. There is also little information about dynamic changes in metabolites and lipids in the cell cycle. Here, the authors present such information for dividing yeast cells.


2018 ◽  
Vol 31 (03) ◽  
pp. 192-198 ◽  
Author(s):  
Grace Chen

AbstractThere is increasing evidence that the gut microbiome, which consists of trillions of microbes representing over 1,000 species of bacteria with over 3 million genes, significantly impacts intestinal health and disease. The gut microbiota not only is capable of promoting intestinal homeostasis and antitumor responses but can also contribute to chronic dysregulated inflammation as well as have genotoxic effects that lead to carcinogenesis. Whether the gut microbiota maintains health or promotes colon cancer may ultimately depend on the composition of the gut microbiome and the balance within the microbial community of protective and detrimental bacterial populations. Disturbances in the normal balanced state of a healthful microbiome, known as dysbiosis, have been observed in patients with colorectal cancer (CRC); however, whether these alterations precede and cause CRC remains to be determined. Nonetheless, studies in mice strongly suggest that the gut microbiota can modulate susceptibility to CRC, and therefore may serve as both biomarkers and therapeutic targets.


1972 ◽  
Vol 130 (1) ◽  
pp. 251-258 ◽  
Author(s):  
Walter Bartley ◽  
Valerie M. Broomhead

1. Saccharomyces cerevisiae cells grown in limiting K+ concentration have their growth inhibited by O2 concentrations above 40%. With these conditions the cells grow very large and are unable to maintain ionic gradients when washed with water. 2. Cells grown in excess of K+ showed the same pattern of change in cell size with change in O2 concentration, but the magnitude of the changes was much less. Cells grown in excess of K+ were not leaky. 3. Cell death, growth and development of ‘leakiness’ were not correlated in the cells grown in limiting K+ concentration. 4. The activities of both alcohol dehydrogenase and cytochrome oxidase were higher in K+-deficient cells than in the cells grown with excess of K+. The differences were much larger when the measurements were made on a cellular basis than when made on a protein basis. 5. In 100% O2 3mm-K+ in the medium was sufficient to produce normal yeast cells.


2011 ◽  
Vol 437 (2) ◽  
pp. 231-241 ◽  
Author(s):  
Ida C. Elle ◽  
Karina T. Simonsen ◽  
Louise C. B. Olsen ◽  
Pernille K. Birck ◽  
Sidse Ehmsen ◽  
...  

ACBP (acyl-CoA-binding protein) is a small primarily cytosolic protein that binds acyl-CoA esters with high specificity and affinity. ACBP has been identified in all eukaryotic species, indicating that it performs a basal cellular function. However, differential tissue expression and the existence of several ACBP paralogues in many eukaryotic species indicate that these proteins serve distinct functions. The nematode Caenorhabditis elegans expresses seven ACBPs: four basal forms and three ACBP domain proteins. We find that each of these paralogues is capable of complementing the growth of ACBP-deficient yeast cells, and that they exhibit distinct temporal and tissue expression patterns in C. elegans. We have obtained loss-of-function mutants for six of these forms. All single mutants display relatively subtle phenotypes; however, we find that functional loss of ACBP-1 leads to reduced triacylglycerol (triglyceride) levels and aberrant lipid droplet morphology and number in the intestine. We also show that worms lacking ACBP-2 show a severe decrease in the β-oxidation of unsaturated fatty acids. A quadruple mutant, lacking all basal ACBPs, is slightly developmentally delayed, displays abnormal intestinal lipid storage, and increased β-oxidation. Collectively, the present results suggest that each of the ACBP paralogues serves a distinct function in C. elegans.


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