Candida albicans CHK1 gene from two-component system is essential for its pathogenicity in oral candidiasis.
Yujie ZhouLei ChengBinyou LiaoYangyang ShiYulong NiuChengguang ZhuXingchen YeXuedong ZhouBiao RenPublished in: Applied microbiology and biotechnology (2021)
The roles of Candida albicans CHK1, a key gene from two-component system, in oral mucosal infection are not clear. This study evaluated the key roles of CHK1 gene in vitro and in vivo. The expression of CHK1 and its regulated virulence factors were tested during the oral epithelial cell infection. The production of lactate dehydrogenase, ROS, and IL-1α combined with the confocal and scanning electron microscope observation was employed to identify the capability of CHK1 in damaging the epithelial cells. Both immunocompetent and immunodeficient mice oropharyngeal infection models were involved to confirm the roles of CHK1 gene in vivo. The expression of CHK1 gene was significantly increased during the oral epithelial cell infection. The chk1Δ/Δ mutant failed to damage the epithelial cells or induce IL-α and ROS production. Interestingly, chk1Δ/Δ can also form the similar hyphae with WT and complementary strains. Accordingly, chk1Δ/Δ did not affect the adhesion and invasion rates of C. albicans to oral epithelial cells. However, chk1Δ/Δ significantly decreased the expression levels of the virulence factors, including ALS2, SAP6, and YWP1. The chk1Δ/Δ also failed to cause oral candidiasis in both immunocompetent and immunodeficient mice indicating that CHK1 gene from the two-component system is essential for the pathogenicity of C. albicans. KEY POINTS: • CHK1gene is essential for C. albicans in oral candidiasis • C. albicans without CHK1 gene can form "non-pathogenic" hyphae. • CHK1 gene regulates the virulence of C. albicans.
Keyphrases
- candida albicans
- biofilm formation
- dna damage response
- copy number
- genome wide
- escherichia coli
- genome wide identification
- poor prognosis
- staphylococcus aureus
- pseudomonas aeruginosa
- dna methylation
- oxidative stress
- metabolic syndrome
- dna damage
- dna repair
- cystic fibrosis
- insulin resistance
- reactive oxygen species
- binding protein
- electron microscopy