ABSTRACT

Introduction: Candida albicans is an opportunistic pathogen that causes oral candidiasis. A previous study showed that Bgl2p and Ecm33p may mediate the interaction between the yeast and saliva-coated hydroxyapatite (SHA; a model for the tooth surface). This study investigated the roles of these cell wall proteins in the adherence of C. albicans to SHA beads.

Methods: C. albicans BGL2 and ECM33 null mutants were generated from wild-type strain SC5314 by using the SAT1-flipper gene disruption method. A novel method based on labelling the yeast with Nile red, was used to investigate the adherence.

Results: Adhesion of bgl2Δ and ecm33Δ null mutants to SHA beads was 76.4% and 64.8% of the wild-type strain, respectively. Interestingly, the adhesion of the bgl2Δ, ecm33Δ double mutant (87.7%) was higher than that of both single mutants. qRT-PCR analysis indicated that the ALS1 gene was over-expressed in the bgl2Δ, ecm33Δ strain. The triple null mutant showed a significantly reduced adherence to the beads, (37.6%), compared to the wild-type strain.

Conclusion: Bgl2p and Ecm33p contributed to the interaction between C. albicans and SHA beads. Deletion of these genes triggered overexpression of the ALS1 gene in the bgl2Δ/ecm33Δ mutant strain, and deletion of all three genes caused a significant decrease in adhesion.

 抽象的

简介：白色念珠菌是一种引起口腔念珠菌病的机会致病菌。之前的一项研究表明，Bgl2p 和 Ecm33p 可能介导酵母和唾液涂层羟基磷灰石（SHA；牙齿表面模型）之间的相互作用。本研究调查了这些细胞壁蛋白在白色念珠菌粘附 SHA 珠子中的作用。

方法：通过使用SAT1 -flipper基因破坏方法从野生型菌株SC5314产生白色念珠菌BGL2和ECM33无效突变体。使用一种基于尼罗红标记酵母的新方法来研究粘附性。

结果： bgl2Δ和ecm33Δ无效突变体对 SHA 珠的粘附力分别是野生型菌株的 76.4% 和 64.8%。有趣的是， bgl2Δ、ecm33Δ双突变体的粘附力（87.7%）高于两个单突变体。 qRT-PCR分析表明ALS1基因在bgl2Δ、ecm33Δ菌株中过表达。与野生型菌株相比，三无效突变体显示出对珠子的粘附显着降低（37.6%）。

结论：Bgl2p 和 Ecm33p 有助于白色念珠菌和 SHA 珠之间的相互作用。这些基因的删除引发了bgl2Δ/ecm33Δ突变株中ALS1基因的过度表达，并且所有三个基因的删除导致粘附力显着下降。