Hall, R.A. and De Sordi, L. and Maccallum, D.M. and Topal, H. and Eaton, R. and Bloor, J.W. and Robinson, Gary K and Levin, L.R. and Buck, J. and Wang, Y. and Gow, N.A.R. and Steegborn, C. and Muhlschlegel, F.A. (2010) CO(2) acts as a signalling molecule in populations of the fungal pathogen Candida albicans. PLoS pathogens, 6 (11). e1001193. ISSN 1553-7374.
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Available under License Creative Commons Attribution.
When colonising host-niches or non-animated medical devices, individual cells of the fungal pathogen Candida albicans expand into significant biomasses. Here we show that within such biomasses, fungal metabolically generated CO(2) acts as a communication molecule promoting the switch from yeast to filamentous growth essential for C. albicans pathology. We find that CO(2)-mediated intra-colony signalling involves the adenylyl cyclase protein (Cyr1p), a multi-sensor recently found to coordinate fungal responses to serum and bacterial peptidoglycan. We further identify Lys 1373 as essential for CO(2)/bicarbonate regulation of Cyr1p. Disruption of the CO(2)/bicarbonate receptor-site interferes selectively with C. albicans filamentation within fungal biomasses. Comparisons between the Drosophila melanogaster infection model and the mouse model of disseminated candidiasis, suggest that metabolic CO(2) sensing may be important for initial colonisation and epithelial invasion. Our results reveal the existence of a gaseous Candida signalling pathway and its molecular mechanism and provide insights into an evolutionary conserved CO(2)-signalling system.
|Divisions:||Faculties > Science Technology and Medical Studies > School of Biosciences > Biomedical Research Group|
|Depositing User:||Sue Davies|
|Date Deposited:||29 Jun 2011 16:35|
|Last Modified:||11 Jun 2012 15:14|
|Resource URI:||http://kar.kent.ac.uk/id/eprint/27488 (The current URI for this page, for reference purposes)|
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