scholarly journals Corrigendum to

Author(s):  
Shuangyan Yao ◽  
Yuting Feng ◽  
Amjad Islam ◽  
Manjari Shrivastava ◽  
Hongcheng Gu ◽  
...  
2000 ◽  
Vol 20 (23) ◽  
pp. 8696-8708 ◽  
Author(s):  
Jiangye Chen ◽  
Song Zhou ◽  
Qin Wang ◽  
Xi Chen ◽  
Ting Pan ◽  
...  

ABSTRACT Both mitogen-activated protein kinases and cyclin-dependent kinases play a role in hyphal development in Candida albicans. Using an oligonucleotide probe-based screen, we have isolated a new member of the Cdc2 kinase subfamily, designated Crk1 (Cdc2-related kinase). The protein sequence of Crk1 is most similar to those ofSaccharomyces cerevisiae Sgv1 and human Pkl1/Cdk9. InS. cerevisiae, CRK1 suppresses some, but not all, of the defects associated with an sgv1 mutant. Deleting both copies of CRK1 in C. albicansslows growth slightly but leads to a profound defect in hyphal development under all conditions examined. crk1/crk1mutants are impaired in the induction of hypha-specific genes and are avirulent in mice. Consistent with this, ectopic expression of the Crk1 kinase domain (CRK1N) promotes filamentous or invasive growth in S. cerevisiae and hyphal development in C. albicans. The activity of Crk1 inS. cerevisiae requires Flo8 but is independent of Ste12 and Phd1. Similarly, Crk1 promotes filamentation through a route independent of Cph1 and Efg1 in C. albicans. RAS1V13 can also activate filamentation in acph1/cph1 efg1/efg1 double mutant. Interestingly,CRK1N produces florid hyphae in ras1/ras1strains, while RAS1V13 generates feeble hyphae in crk1/crk1 strains.


2020 ◽  
Vol 18 ◽  
pp. 4002-4015
Author(s):  
Shuangyan Yao ◽  
Yuting Feng ◽  
Amjad Islam ◽  
Manjari Shrivastava ◽  
Hongcheng Gu ◽  
...  

2010 ◽  
Vol 9 (9) ◽  
pp. 1320-1328 ◽  
Author(s):  
Patricia L. Carlisle ◽  
David Kadosh

ABSTRACT The ability of Candida albicans, the most common human fungal pathogen, to transition from yeast to hyphae is essential for pathogenicity. While a variety of transcription factors important for filamentation have been identified and characterized, links between transcriptional regulators of C. albicans morphogenesis and molecular mechanisms that drive hyphal growth are not well defined. We have previously observed that constitutive expression of UME6, which encodes a filament-specific transcriptional regulator, is sufficient to direct hyphal growth in the absence of filament-inducing conditions. Here we show that HGC1, encoding a cyclin-related protein necessary for hyphal growth under filament-inducing conditions, is specifically important for agar invasion, hyphal extension, and formation of true septa in response to constitutive UME6 expression under non-filament-inducing conditions. HGC1-dependent inactivation of Rga2, a Cdc42 GTPase activating protein (GAP), also appears to be important for these processes. In response to filament-inducing conditions, HGC1 is induced prior to UME6 although UME6 controls the level and duration of HGC1 expression, which are likely to be important for hyphal extension. Interestingly, an epistasis analysis suggests that UME6 and HGC1 play distinct roles during early filament formation. These findings establish a link between a key regulator of filamentation and a downstream mechanism important for hyphal formation. In addition, this study demonstrates that a strain expressing constitutive high levels of UME6 provides a powerful strategy to specifically dissect downstream mechanisms important for hyphal development in the absence of complex filament-inducing conditions.


PLoS Genetics ◽  
2009 ◽  
Vol 5 (9) ◽  
pp. e1000664 ◽  
Author(s):  
Sarah L. Elson ◽  
Suzanne M. Noble ◽  
Norma V. Solis ◽  
Scott G. Filler ◽  
Alexander D. Johnson

2010 ◽  
Vol 165 (3) ◽  
pp. 250-258 ◽  
Author(s):  
Peter Hayek ◽  
Leila Dib ◽  
Pascal Yazbeck ◽  
Berna Beyrouthy ◽  
Roy A. Khalaf

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chew Teng Tan ◽  
Xiaoli Xu ◽  
Yuan Qiao ◽  
Yue Wang

AbstractThe commensal fungus Candida albicans often causes life-threatening infections in patients who are immunocompromised with high mortality. A prominent but poorly understood risk factor for the C. albicans commensal‒pathogen transition is the use of broad-spectrum antibiotics. Here, we report that β-lactam antibiotics cause bacteria to release significant quantities of peptidoglycan fragments that potently induce the invasive hyphal growth of C. albicans. We identify several active peptidoglycan subunits, including tracheal cytotoxin, a molecule produced by many Gram-negative bacteria, and fragments purified from the cell wall of Gram-positive Staphylococcus aureus. Feeding mice with β-lactam antibiotics causes a peptidoglycan storm that transforms the gut from a niche usually restraining C. albicans in the commensal state to promoting invasive growth, leading to systemic dissemination. Our findings reveal a mechanism underlying a significant risk factor for C. albicans infection, which could inform clinicians regarding future antibiotic selection to minimize this deadly disease incidence.


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