Homologous recombination in <i>Candida albicans</i>: role of CaRad52p in DNA repair, integration of linear DNA fragments and telomere length

Ciudad, Toni; Andaluz, Encarnación; Steinberg-Neifach, Olga; Lue, Neal F.; Gow, Neil A. R.; Calderone, Richard; Larriba, Germán

doi:10.1111/j.1365-2958.2004.04197.x

Cited by 56 publications

(76 citation statements)

References 89 publications

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“…Miller & Sarachek (1974) concluded that C. albicans does not possess a photoreactivating enzyme. We searched the genome sequence of C. albicans for photolyase homologues and did not find any good candidates, in agreement with an earlier report of a BLAST search of the C. albicans genome (Ciudad et al, 2004). However, a photoreactivation activity could be masked by a very efficient NER pathway, which would be uncovered by the NER mutants.…”

Section: Susceptibility To Dna-damaging Agentssupporting

confidence: 66%

Analysis of base excision and nucleotide excision repair in Candida albicans

et al. 2008

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Candida albicans, clinically the most important human fungal pathogen, rapidly develops resistance to antifungal drugs. The acquisition of resistance has been linked to various types of genome changes. As part of an ongoing study of this problem, we investigated mutation, genome stability and drug resistance acquisition in C. albicans strains with deletions in the base excision repair (BER) genes NTG1, APN1 and OGG1, and in the nucleotide excision repair (NER) genes RAD2 and RAD10. The BER mutants did not exhibit any change in their susceptibility to DNA-damaging agents, but the NER mutants were extremely sensitive to UV-induced DNA damage. We did not observe any significant change in mutation, genome stability and antifungal drug sensitivity in the mutant strains we tested. However, we detected a number of intriguing phenotypic differences between strains bearing deletions in equivalent C. albicans and Saccharomyces cerevisiae BER and NER genes, which may be related to differences in the life cycles of these two fungi.

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Section: Susceptibility To Dna-damaging Agentssupporting

confidence: 66%

Analysis of base excision and nucleotide excision repair in Candida albicans

et al. 2008

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“…Two conserved proteins integral to homologous recombination in Saccharomyces cerevisiae and higher eukaryotes are Rad51p and Rad52p (Krogh and Symington, 2004). C. albicans Rad52p has also been shown to be critical for survival in the presence of DNA damaging agents such as MMS (Ciudad et al, 2004). Based on its homology to S. cerevisiae RAD51, orf19.3752 has been designated C. albicans RAD51, with a putative role in homologous recombination (candidagenome.org).…”

Section: Deletion Of Rad51 or Rad52 Results In Increased White-opaquementioning

confidence: 99%

“…In C. albicans, as in many fungi, DNA repair is often mediated through homologous recombination (Ciudad et al, 2004;Krogh and Symington, 2004). Two conserved proteins integral to homologous recombination in Saccharomyces cerevisiae and higher eukaryotes are Rad51p and Rad52p (Krogh and Symington, 2004).…”

Section: Deletion Of Rad51 or Rad52 Results In Increased White-opaquementioning

confidence: 99%

Stress-Induced Phenotypic Switching inCandida albicans

Alby

Bennett

2009

MBoC

111

108

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Candida albicans is both a common commensal and an opportunistic pathogen, being a prevalent cause of mucosal and systemic infections in humans. Phenotypic switching between white and opaque forms is a reversible transition that influences virulence, mating behavior, and biofilm formation. In this work, we show that a wide range of factors induces high rates of switching from white to opaque. These factors include different forms of environmental stimuli such as genotoxic and oxidative stress, as well as intrinsic factors such as mutations in DNA repair genes. We propose that these factors increase switching to the opaque phase via a common mechanism-inhibition of cell growth. To confirm this hypothesis, growth rates were artificially manipulated by varying expression of the CLB4 cyclin gene; slowing cell growth by depleting CLB4 resulted in a concomitant increase in white-opaque switching. Furthermore, two clinical isolates of C. albicans, P37005 and L26, were found to naturally exhibit both slow growth and high rates of white-opaque switching. Notably, suppression of the slow growth phenotype suppressed hyperswitching in the P37005 isolate. Based on the sensitivity of the switch to levels of the master regulator Wor1, we propose a model for how changes in cellular growth modulate white-opaque switching frequencies.

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“…After incubation at 30°C for 72 h, the colony-forming units were determined as described previously (Ciudad et al, 2004).…”

Section: Dna Damage Assaymentioning

confidence: 99%

Efg1-mediated Recruitment of NuA4 to Promoters Is Required for Hypha-specific Swi/Snf Binding and Activation inCandida albicans

Lü

Mao

et al. 2008

MBoC

102

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Efg1 is essential for hyphal development and virulence in the human pathogenic fungus Candida albicans. How Efg1 regulates gene expression is unknown. Here, we show that Efg1 interacts with components of the nucleosome acetyltransferase of H4 (NuA4) histone acetyltransferase (HAT) complex in both yeast and hyphal cells. Deleting YNG2, a subunit of the NuA4 HAT module, results in a significant decrease in the acetylation level of nucleosomal H4 and a profound defect in hyphal development, as well as a defect in the expression of hypha-specific genes. Using chromatin immunoprecipitation, Efg1 and the NuA4 complex are found at the UAS regions of hypha-specific genes in both yeast and hyphal cells, and Efg1 is required for the recruitment of NuA4. Nucleosomal H4 acetylation at the promoters peaks during initial hyphal induction in an Efg1-dependent manner. We also find that Efg1 bound to the promoters of hypha-specific genes is critical for recruitment of the Swi/Snf chromatin remodeling complex during hyphal induction. Our data show that the recruitment of the NuA4 complex by Efg1 to the promoters of hypha-specific genes is required for nucleosomal H4 acetylation at the promoters during hyphal induction and for subsequent binding of Swi/Snf and transcriptional activation. INTRODUCTIONCandida albicans has emerged as one of the most prevalent opportunistic fungal pathogens in humans. It causes mucosal as well as systemic candidiasis, especially in immunocompromised patients. C. albicans can undergo reversible morphogenetic transitions between budding yeast, pseudohyphal, and hyphal growth forms. Its unique ability to switch from yeast to hyphal growth in response to various signals is essential for its pathogenicity.Central to the yeast-to-hypha transition is the transcription factor Efg1, a member of the Asm1p, Phd1p, Sok2p, Efg1p, and StuAp (APSES) family of fungal proteins that regulate cellular differentiation in ascomycetes. Members of this family share a conserved DNA binding domain. Efg1 is an essential regulator of hyphal development, chlamydospore formation, and white-opaque phenotypic switching in C. albicans (Lo et al., 1997;Stoldt et al., 1997;Sonneborn et al., 1999;Srikantha et al., 2000;Zordan et al., 2007). It is suggested to function downstream of the cAMP/protein kinase A (PKA) pathway in hyphal development (Sonneborn et al., 2000;Bockmuhl and Ernst, 2001), and both Efg1 and PKA are required for the induction of hypha-specific genes. However, Efg1 also regulates other genes that are not modulated by the cAMP pathway (Sohn et al., 2003;Doedt et al., 2004;Harcus et al., 2004;Setiadi et al., 2006). Numerous in vitro and in vivo studies with efg1 mutants have demonstrated that Efg1 is important for C. albicans virulence and for the interactions of C. albicans with endothelial and epithelia cells, as well as biofilm formation and catheter infection (Lo et al., 1997;Phan et al., 2000;Dieterich et al., 2002;Lewis et al., 2002;Ramage et al., 2002;Garcia-Sanchez et al., 2004). Despite its importance, molecula...

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Homologous recombination in Candida albicans: role of CaRad52p in DNA repair, integration of linear DNA fragments and telomere length

Cited by 56 publications

References 89 publications

Analysis of base excision and nucleotide excision repair in Candida albicans

Analysis of base excision and nucleotide excision repair in Candida albicans

Stress-Induced Phenotypic Switching inCandida albicans

Efg1-mediated Recruitment of NuA4 to Promoters Is Required for Hypha-specific Swi/Snf Binding and Activation inCandida albicans

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