Display options
Cite
Ng TS, Chew SY, Rangasamy P, et al. SNF3 as High Affinity Glucose Sensor and Its Function in Supporting the Viability of Candida glabrata under Glucose-Limited Environment. Front Microbiol. 2015;6:1334doi: 10.3389/fmicb.2015.01334.
Ng, T. S., Chew, S. Y., Rangasamy, P., Mohd Desa, M. N., Sandai, D., Chong, P. P., & Than, L. T. (2015). SNF3 as High Affinity Glucose Sensor and Its Function in Supporting the Viability of Candida glabrata under Glucose-Limited Environment. Frontiers in microbiology, 61334. https://doi.org/10.3389/fmicb.2015.01334
Ng, Tzu Shan, et al. "SNF3 as High Affinity Glucose Sensor and Its Function in Supporting the Viability of Candida glabrata under Glucose-Limited Environment." Frontiers in microbiology vol. 6 (2015): 1334. doi: https://doi.org/10.3389/fmicb.2015.01334
Ng TS, Chew SY, Rangasamy P, Mohd Desa MN, Sandai D, Chong PP, Than LT. SNF3 as High Affinity Glucose Sensor and Its Function in Supporting the Viability of Candida glabrata under Glucose-Limited Environment. Front Microbiol. 2015 Dec 01;6:1334. doi: 10.3389/fmicb.2015.01334. eCollection 2015. PMID: 26648919; PMCID: PMC4664639.
Copy Download .nbib Format: NLM
Share it on

Front Microbiol. 2015 Dec 01;6:1334. doi: 10.3389/fmicb.2015.01334. eCollection 2015.

SNF3 as High Affinity Glucose Sensor and Its Function in Supporting the Viability of Candida glabrata under Glucose-Limited Environment.

Frontiers in microbiology

Tzu Shan Ng, Shu Yih Chew, Premmala Rangasamy, Mohd N Mohd Desa, Doblin Sandai, Pei Pei Chong, Leslie Thian Lung Than

Affiliations

  1. Department of Medical Microbiology and Parasitology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia Serdang, Malaysia.
  2. Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia Serdang, Malaysia.
  3. Infectomics Cluster, Advanced Medical and Dental Institute, Universiti Sains Malaysia Bertam, Malaysia.

PMID: 26648919 PMCID: PMC4664639 DOI: 10.3389/fmicb.2015.01334

Abstract

Candida glabrata is an emerging human fungal pathogen that has efficacious nutrient sensing and responsiveness ability. It can be seen through its ability to thrive in diverse range of nutrient limited-human anatomical sites. Therefore, nutrient sensing particularly glucose sensing is thought to be crucial in contributing to the development and fitness of the pathogen. This study aimed to elucidate the role of SNF3 (Sucrose Non Fermenting 3) as a glucose sensor and its possible role in contributing to the fitness and survivability of C. glabrata in glucose-limited environment. The SNF3 knockout strain was constructed and subjected to different glucose concentrations to evaluate its growth, biofilm formation, amphotericin B susceptibility, ex vivo survivability and effects on the transcriptional profiling of the sugar receptor repressor (SRR) pathway-related genes. The CgSNF3Δ strain showed a retarded growth in low glucose environments (0.01 and 0.1%) in both fermentation and respiration-preferred conditions but grew well in high glucose concentration environments (1 and 2%). It was also found to be more susceptible to amphotericin B in low glucose environment (0.1%) and macrophage engulfment but showed no difference in the biofilm formation capability. The deletion of SNF3 also resulted in the down-regulation of about half of hexose transporters genes (four out of nine). Overall, the deletion of SNF3 causes significant reduction in the ability of C. glabrata to sense limited surrounding glucose and consequently disrupts its competency to transport and perform the uptake of this critical nutrient. This study highlighted the role of SNF3 as a high affinity glucose sensor and its role in aiding the survivability of C. glabrata particularly in glucose limited environment.

Keywords: Candida glabrata; SNF3; glucose sensor; glucose-limited environment; hexose transporter

References

  1. Genetics. 1999 Mar;151(3):979-87 - PubMed
  2. Mol Cell Biol. 1999 Jul;19(7):4561-71 - PubMed
  3. Microbiol Mol Biol Rev. 1999 Sep;63(3):554-69 - PubMed
  4. Nucleic Acids Res. 2001 May 1;29(9):e45 - PubMed
  5. Nucleic Acids Res. 2002 May 1;30(9):e36 - PubMed
  6. Methods Enzymol. 2002;350:3-41 - PubMed
  7. FEMS Yeast Res. 2002 May;2(2):183-201 - PubMed
  8. Anal Biochem. 2003 Nov 15;322(2):287-91 - PubMed
  9. J Antimicrob Chemother. 2004 Aug;54(2):376-85 - PubMed
  10. Antimicrob Agents Chemother. 2005 Jun;49(6):2226-36 - PubMed
  11. Appl Environ Microbiol. 1990 Jan;56(1):281-7 - PubMed
  12. Microbiol Mol Biol Rev. 2006 Mar;70(1):253-82 - PubMed
  13. J Biol Chem. 2006 Sep 8;281(36):26144-9 - PubMed
  14. Eukaryot Cell. 2006 Oct;5(10):1726-37 - PubMed
  15. Obstet Gynecol. 2006 Dec;108(6):1432-7 - PubMed
  16. Proc Natl Acad Sci U S A. 2007 May 1;104(18):7628-33 - PubMed
  17. FEMS Microbiol Rev. 2008 Jul;32(4):673-704 - PubMed
  18. Nat Protoc. 2008;3(9):1494-500 - PubMed
  19. FEMS Yeast Res. 2009 Jun;9(4):526-34 - PubMed
  20. Mol Biol Cell. 2009 Nov;20(22):4845-55 - PubMed
  21. Cell Microbiol. 2010 Feb;12(2):199-216 - PubMed
  22. PLoS Pathog. 2010 Mar 26;6(3):e1000828 - PubMed
  23. Int J Med Microbiol. 2011 Jun;301(5):400-7 - PubMed
  24. Cell Microbiol. 2012 Sep;14(9):1319-35 - PubMed
  25. BMC Mol Biol. 2012 Jun 29;13:22 - PubMed
  26. MBio. 2012 Dec 11;3(6):null - PubMed
  27. PLoS One. 2013 May 14;8(5):e64239 - PubMed
  28. PLoS One. 2014 Apr 22;9(4):e96203 - PubMed
  29. Infect Genet Evol. 2016 Jun;40:331-338 - PubMed
  30. Front Microbiol. 2015 Sep 04;6:919 - PubMed
  31. Jundishapur J Microbiol. 2015 Nov 21;8(11):e25177 - PubMed
  32. EMBO J. 1998 May 1;17(9):2566-73 - PubMed

Publication Types