Advances in gene knockout technology of Candida albicans

Abstract

Abstract:

Nowadays,candidiasis has been one of the most common hospital-acquired infection,and Candida albicans is the most important pathogen.As C.albicans is capable of developing drug-resistance, understanding the overall mechanism of C.albicans pathogenesis, and further finding new drug targets are important goals. To study this pathogen, it is advantageous to manipulate its genome. This review focused on recent progress of C.albicans gene knockout strategies, and discussed their merits and drawbacks.

Key words: Candida albicans, gene knockout, selectable marker, RNA interference

CLC Number:

R 379.4

TAN Hong-yue, CHEN Li-hua, HUANG You-ming, ZHU Hong-mei, GU Jun, WEN Hai. Advances in gene knockout technology of Candida albicans[J]. Chinese Journal of Mycology, 2012, 7(6): 375-379.

References

[1] Schelenz S, Abdallah S, Gray G, et al. Epidemiology of oral yeast colonization and infection in patients with hematological malignancies, head neck and solid tumors
[J]. J Oral Pathol Med,2011,40(1):83-89.

[2] 吴绍熙,郭宁如. 深部真菌感染的诊断与治疗
[J].抗真菌药物与真菌感染诊治研究学术会议论文集,2003:21-30.

[3] Shingu-Vazquez M, Traven A. Mitochondria and fungal pathogenesis: drug tolerance, virulence, and potential for antifungal therapy
[J]. Eukaryot Cell,2011,10(11):1376-1383.

[4] Noble SM, Johnson AD. Genetics of Candida albicans, a diploid human fungal pathogen
[J]. Annu Rev Genet,2007,41:193-211.

[5] Barnett JA. A history of research on yeasts 12: medical yeasts Part 1, Candida albicans
[J]. Yeast,2008,25(6):385-417.

[6] Magee PT, Gale C, Berman J, et al. Molecular genetic and genomic approaches to the study of medically important fungi
[J]. Infect Immun,2003,71(5):2299-2309.

[7] Fonzi WA, Irwin MY. Isogenic strain construction and gene mapping in Candida albicans
[J]. Genetics,1993,134(3):717-728.

[8] Lay J, Henry LK, Clifford J, et al. Altered expression of selectable marker URA3 in gene-disrupted Candida albicans strains complicates interpretation of virulence studies
[J]. Infect Immun,1998,66(11):5301-5306.

[9] García MG, O'Connor JE, García LL. Isolation of a Candida albicans gene, tightly linked to URA3, coding for a putative transcription factor that suppresses a Saccharomyces cerevisiae aft1 mutation
[J]. Yeast,2001,18(4):301-311.

[10] Ramanan N, Wang Y. A high-affinity iron permease essential for Candida albicans virulence
[J]. Science,2000,288(5468):1062-1064.

[11] Brand A, MacCallum DM, Brown AJP, et al. Ectopic expression of URA3 can influence the virulence phenotypes and proteome of Candida albicans but can be overcome by targeted reintegration of URA3 at the RSP10 locus
[J]. Eukaryot Cell,2004,3(4):900-909.

[12] Cox MM, Layton SL, Jiang T. Scarle and site-directed mutagenesis in Salmonella enteritidis chromosome
[J]. BMC Biotechnol,2007,7:59.

[13] Liang R, Liu J. Scarless and sequential gene modification in Pseudomonas using PCR product flanked by short homology regions
[J]. BMC Microbiol,2010,10:209.

[14] Wellington M, Kabir MA, Rustchenko E. 5-Fluoro-orotic acid induces chromosome alterations in genetically manipulated strains of Candida albicans
[J]. Mycologia,2006, 98(3):393-398.

[15] Cheng S, Nguyen MH, Zhang Z, et al. Evaluation of the roles of four Candida albicans genes in virulence by using gene disruption strains that express URA3 from the native locus
[J]. Infect Immun,2003,71(10):6101-6103.

[16] Ramón AM, Fonzi WA. Diverged binding specificity of Rim101p, the Candida albicans ortholog of PacC
[J]. Eukaryot Cell,2003,2(4):718-728.

[17] Morschhäuser J, Michel S, Staib P. Sequential gene disruption in Candida albicans by FLP-mediated site-specific recombination
[J]. Mol Microbiol,1999,32(3):547- 556.

[18] Negredo A, Monteoliva L, Gil C, et al. Cloning, analysis and one-step disruption of the ARG5,6 gene of Candida albicans
[J]. Microbiology,1997,143(Pt2):297-302.

[19] Wilson RB, Davis D, Mitchell AP. Rapid hypothesis testing with Candida albicans through gene disruption with short homology regions
[J]. J Bacteriol,1999,181(6):1868-1874.

[20] Enloe B, Diamond A, Mitchell AP. A single-transformation gene function test in diploid Candida albicans
[J]. J Bacteriol,2000,182(20):5730-5736.

[21] Noble SM, Johnson AD. Strains and strategies for large-scale gene deletion studies of the diploid human fungal pathogen Candida albicans
[J]. Eukaryot Cell,2005,4(2):298-309.

[22] Dennison PM, Ramsdale M, Manson CL, et al. Gene disruption in Candida albicans using a synthetic, codon-optimised Cre-loxP system
[J]. Fungal Genet Biol,2005,42(9): 737-748.

[23] Heilmann CJ, Schneider S, Barker KS, et al. An A643T mutation in the transcription factor Upc2p causes constitutive ERG11 upregulation and increased fluconazole resistance in Candida albicans
[J].Antimicrob Agents Chemother,2010,54(1):353-359.

[24] Goshorn AK, Scherer S. Genetic analysis of prototrophic natural variants of Candida albicans
[J]. Genetics,1989,123(4):667-673.

[25] Wirsching S, Michel S, Morschhäuser J. Targeted gene disruption in Candida albicans wild-type strains: the role of the MDR1 gene in fluconazole resistance of clinical Candida albicans isolates
[J]. Mol Microbiol,2000,36(4):856-865.

[26] Reuss O, Vik A, Kolter R, et al. The SAT1 flipper, an optimized tool for gene disruption in Candida albicans
[J]. Gene,2004,341:119-127.

[27] Shen J, Guo W, Köhler JR. CaNAT1, a heterologous dominant selectable marker for transformation of Candida albicans and other pathogenic Candida species
[J]. Infect Immun,2005,73(2):1239-1242.

[28] Samaranayake DP, Hanes SD. Milestones in Candida albicans gene manipulation
[J]. Fungal Genet Biol,2011,48(9):858-865.

[29] 胡辉,张永信.一种用于白念珠菌基因敲除的新型载体的构建
[J].中华传染病杂志,2009,27(2):65-68.

[30] Liu H, Cottrell TR, Pierini LM, et al. RNA interference in the pathogenic fungus Cryptococcus neoformans
[J]. Genetics,2002,160(2):463-470.

[31] Mouyna I, Henry C, Doering TL, et al. Gene silencing with RNA interference in the human pathogenic fungus Aspergillus fumigatus
[J]. FEMS Microbiol Lett,2004,237(2): 317-324.

[32] Barton LM, Prade RA. Inducible RNA interference of brlAb in Aspergillus nidulans
[J]. Eukaryot Cell,2008,7(11):2004-2007.

[33] Drinnenberg IA, Weinberg DE, Xie KT, et al. RNAi in budding yeast
[J]. Science,2009, 326(5952):544-550.

[34] Staab JF, White TC, Marr KA. Hairpin dsRNA does not trigger RNA interference in Candida albicans cells
[J]. Yeast,2011,28(1):1-8.

[35] Moazeni M, Khoramizadeh MR, Kordbacheh P,et al. RNA-Mediated Gene Silencing in Candida albicans: Inhibition of Hyphae Formation by Use of RNAi Technology
[J]. Mycopathologia,2012,174(3):177-185.

[36] Storici F, Lewis LK, Resnick MA.In vivo site-directed mutagenesis using oligonucleotides
[J]. Nat Biotechnol,2001,19(8):773-776.

[37] Storici F, Resnick MA. The delitto perfetto approach to in vivo site-directed mutagenesis and chromosome rearrangements with synthetic oligonucleotides in yeast
[J]. Methods Enzymol,2006,409:329-345.

[38] Homann OR, Dea J, Noble SM, et al. A phenotypic profile of the Candida albicans regulatory network
[J]. PLoS Genet,2009,5(12):e1000783.

[39] Noble SM, French S, Kohn LA, et al. Systematic screens of a Candida albicans homozygous deletion library decouple morphogenetic switching and pathogenicity
[J]. Nat Genet,2010,42(7):590-598.