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N-acetylglucosamine (GlcNAc) inducible gene, GIG2, is a novel component of GlcNAc metabolism in Candida albicans

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Title N-acetylglucosamine (GlcNAc) inducible gene, GIG2, is a novel component of GlcNAc metabolism in Candida albicans
 
Creator Ghosh, Swagata
Rao, Kongara Hanumantha
Bhavesh, Neel Sarovar
Das, Gobardhan
Dwivedi, Ved Prakash
Datta, Asis
 
Subject Candida albicans
 
Description Accepted date: 22 October 2013
Candida albicans is an opportunistic fungal pathogen that resides in the human body as a commensal and can turn pathogenic when the host is immunocompromised. Adaptation of C. albicans to host niche-specific conditions is important for the establishment of pathogenicity, where the ability of C. albicans to utilize multiple carbon sources provides additional flexibility. One alternative sugar is N-acetylglucosamine (GlcNAc), which is now established as an important carbon source for many pathogens and can also act as a signaling molecule. Although GlcNAc catabolism has been well studied in many pathogens, the importance of several enzymes involved in the formation of metabolic intermediates still remains elusive. In this context, microarray analysis was carried out to investigate the transcriptional responses induced by GlcNAc under different conditions. A novel gene that was highly upregulated immediately following the GlcNAc catabolic genes was identified and was named GIG2 (GlcNAc-induced gene 2). This gene is regulated in a manner distinct from that of the GlcNAc-induced genes described previously in that GlcNAc metabolism is essential for its induction. Furthermore, this gene is involved in the metabolism of N-acetylneuraminate (sialic acid), a molecule equally important for initial host-pathogen recognition. Mutant cells showed a considerable decrease in fungal burden in mouse kidneys and were hypersensitive to oxidative stress conditions. Since GIG2 is also present in many other fungal and enterobacterial genomes, targeted inhibition of its activity would offer insight into the treatment of candidiasis and other fungal or enterobacterial infections.
We thank Cheryl Gale, Masakazu Niimi, Janet Quinn, James B. Konopka,
A. D. Johnson, and Alistair J. P. Brown for generously providing the plasmids and C. albicans strains used in this study. We also thank A. K. Dinda,
AIIMS, New Delhi, India, for his kind help in performing histopathological studies. P. M. N. Rajesh, Waters India Pvt. Ltd., Bangalore, India,
helped with the UPLC-coupled MS analysis. The Confocal Microscope
Facility at NIPGR is acknowledged for the confocal data.
We thank the Department of Biotechnology (DBT), Government of
India, for providing financial support toward the procurement of 500-
MHz and 700-MHz NMR spectrometers at the ICGEB and NII, New
Delhi, India. S.G. and K.H.R. are recipients of a CSIR-SRA fellowship.
 
Date 2015-12-16T05:19:53Z
2015-12-16T05:19:53Z
2014
 
Type Article
 
Identifier Eukaryot. Cell, 13(1): 66-76
1535-9778
http://172.16.0.77:8080/jspui/handle/123456789/408
http://ec.asm.org/content/13/1/66.long
10.1128/EC.00244-13
 
Language en_US
 
Publisher American Society for Microbiology