Candida albicans biofilm-defective mutants

被引:121
作者
Richard, ML
Nobile, CJ
Bruno, VM
Mitchell, AP
机构
[1] Columbia Univ, Dept Microbiol, New York, NY 10032 USA
[2] Columbia Univ, Dept Biol Sci, Biol Sci Program, New York, NY 10027 USA
[3] Columbia Univ, Program Cellular Mol & Biophys Studies, New York, NY 10032 USA
关键词
D O I
10.1128/EC.4.8.1493-1502.2005
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Biofilm formation plays a key role in the life cycles and subsistence of many microorganisms. For the human fungal pathogen Candida albicans, biofilm development is arguably a virulence trait, because medical implants that serve as biofilm substrates are significant risk factors for infection. The development of C. albicans biofilms in vitro proceeds through an early phase, in which yeast cells populate a substrate, an intermediate phase, in which pseudohyphal and hyphal cell types are produced, and a maturation phase, in which continued cell growth is accompanied by accumulation of an extracellular matrix. Here we report the results of a screen for C. albicans biofilm-defective mutants, in which homozygous insertions in NUP85, MDS3, KEM1, and SUV3 were found to block biofilm development. Confocal microscopic examination suggests that nup85, suv3, and mds3 mutations cause early-phase arrest, whereas the kem1 mutation causes intermediate-phase arrest. All of the mutants are defective in hypha production in several media. Analysis of mixed-biofilm development indicates that all of the mutants are defective in the production of hyphae in the context of a biofilm. Because all of the mutants are defective in the retention of cells in the biofilm, we infer that hyphae provide an adherent scaffold that stabilizes the biofilm structure.
引用
收藏
页码:1493 / 1502
页数:10
相关论文
共 55 条
[1]   Role of dimorphism in the development of Candida albicans biofilms [J].
Baillie, GS ;
Douglas, LJ .
JOURNAL OF MEDICAL MICROBIOLOGY, 1999, 48 (07) :671-679
[2]   Regulation of azole drug susceptibility by Candida albicans protein kinase CK2 [J].
Bruno, VM ;
Mitchell, AP .
MOLECULAR MICROBIOLOGY, 2005, 56 (02) :559-573
[3]   Large-scale gene function analysis in Candida albicans [J].
Bruno, VM ;
Mitchell, AP .
TRENDS IN MICROBIOLOGY, 2004, 12 (04) :157-161
[4]   Biofilm formation by the fungal pathogen Candida albicans:: Development, architecture, and drug resistance [J].
Chandra, J ;
Kuhn, DM ;
Mukherjee, PK ;
Hoyer, LL ;
McCormick, T ;
Ghannoum, MA .
JOURNAL OF BACTERIOLOGY, 2001, 183 (18) :5385-5394
[5]   Bacterial invasion: The paradigms of enteroinvasive pathogens [J].
Cossart, P ;
Sansonetti, PJ .
SCIENCE, 2004, 304 (5668) :242-248
[6]   Microbial biofilms: from ecology to molecular genetics [J].
Davey, ME ;
O'toole, GA .
MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, 2000, 64 (04) :847-+
[7]   Candida albicans RIM101 pH response pathway is required for host-pathogen interactions [J].
Davis, D ;
Edwards, JE ;
Mitchell, AP ;
Ibrahim, AS .
INFECTION AND IMMUNITY, 2000, 68 (10) :5953-5959
[8]  
Davis DA, 2002, GENETICS, V162, P1573
[9]   Candida biofilms and their role in infection [J].
Douglas, LJ .
TRENDS IN MICROBIOLOGY, 2003, 11 (01) :30-36
[10]   Candida albicans Als1p:: an adhesin that is a downstream effector of the EFG1 filamentation pathway [J].
Fu, Y ;
Ibrahim, AS ;
Sheppard, DC ;
Chen, YC ;
French, SW ;
Cutler, JE ;
Filler, SG ;
Edwards, JE .
MOLECULAR MICROBIOLOGY, 2002, 44 (01) :61-72